TY  - JOUR
AU  - Adžić, Miroslav
AU  - Brkić, Željka
AU  - Bulajić, Sonja
AU  - Mitić, Miloš
AU  - Radojčić, Marija
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1304
AB  - Mitochondria are cell organelles crucial to the production of cellular energy. Several lines of evidence have indicated that mitochondrial dysfunction could be related to the pathophysiology of CNS diseases including bipolar disorder, major depressive disorder, and schizophrenia. These changes include impaired energy metabolism in the brain, co-morbidity with mitochondrial diseases, the effects of psychotropics on mitochondrial function, increased mitochondrial DNA (mtDNA) deletion in the brain, and association with mtDNA polymorphisms. Additionally, psychotropic drug treatments can alter energy metabolism and may affect mitochondrial processes. This review focuses on recent findings regarding the effects of antidepressants on mitochondrial processes in psychiatric disorders. Drug Dev Res 77 : 400-406, 2016. (c) 2016 Wiley Periodicals, Inc.
T2  - Drug Development Research
T1  - Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders
VL  - 77
IS  - 7
SP  - 400
EP  - 406
DO  - 10.1002/ddr.21332
ER  - 

@article{
author = "Adžić, Miroslav and Brkić, Željka and Bulajić, Sonja and Mitić, Miloš and Radojčić, Marija",
year = "2016",
abstract = "Mitochondria are cell organelles crucial to the production of cellular energy. Several lines of evidence have indicated that mitochondrial dysfunction could be related to the pathophysiology of CNS diseases including bipolar disorder, major depressive disorder, and schizophrenia. These changes include impaired energy metabolism in the brain, co-morbidity with mitochondrial diseases, the effects of psychotropics on mitochondrial function, increased mitochondrial DNA (mtDNA) deletion in the brain, and association with mtDNA polymorphisms. Additionally, psychotropic drug treatments can alter energy metabolism and may affect mitochondrial processes. This review focuses on recent findings regarding the effects of antidepressants on mitochondrial processes in psychiatric disorders. Drug Dev Res 77 : 400-406, 2016. (c) 2016 Wiley Periodicals, Inc.",
journal = "Drug Development Research",
title = "Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders",
volume = "77",
number = "7",
pages = "400-406",
doi = "10.1002/ddr.21332"
}

Adžić, M., Brkić, Ž., Bulajić, S., Mitić, M.,& Radojčić, M.. (2016). Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders. in Drug Development Research, 77(7), 400-406.
https://doi.org/10.1002/ddr.21332

Adžić M, Brkić Ž, Bulajić S, Mitić M, Radojčić M. Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders. in Drug Development Research. 2016;77(7):400-406.
doi:10.1002/ddr.21332 .

Adžić, Miroslav, Brkić, Željka, Bulajić, Sonja, Mitić, Miloš, Radojčić, Marija, "Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders" in Drug Development Research, 77, no. 7 (2016):400-406,
https://doi.org/10.1002/ddr.21332 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Brkić, Željka
AU  - Lukić, Iva
AU  - Radojčić, Marija
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/670
AB  - Peripheral inflammation induced by lipopolysaccharide (LPS) causes behavioural changes indicative for depression. The possible mechanisms involve the interference with neuroinflammatory, neuroendocrine, and neurotrophic processes. Apart from heterogeneity in the molecular background, sexual context may be another factor relevant to the manifestation of mood disturbances upon an immune challenge. We investigated sex-dependent effects of a 7-day LPS treatment of adult Wistar rats on depressive-like behaviour and their relation with hypothalamic neuroendocrine factor, corticotrophin-releasing hormone (CRH), proplastic brain-derived neurotropic factor (BDNF), pro-inflammatory cyclooxygenase-2 (COX-2) and nuclear factor kappa beta (NFkB). Also, their regulators, the glucocorticoid receptor (GR) and CCAAT enhancer-binding protein (C/EBP) beta were followed. LPS induced depressive-like behaviour in females was associated with the increased hypothalamic CRH and decreased BDNF, but not with COX-2. These changes were paralleled by an increase in nuclear GR, NFkB and 20 kDa C/EBP beta. LPS also altered behaviour in males and increased CRH expression, but in contrast to females, this was accompanied with the elevated COX-2, accumulation of cytosolic GR and elevated nuclear 38 kDa C/EBP beta and NFkB. In conclusion, depressive-like phenotype induced by LPS in both sexes emerges from similar HPA axis activation and sex-specific alterations of hypothalamic molecular signalling: in males it is related to compromised control of neuroinflamation connected with cytoplasmic GR retention, while in females it is related to diminished proplastic capacity of BDNF. Sex-dependent mechanisms by which inflammation alters hypothalamic processes and cause pathological behaviour in animals, could be operative in the treatment of depression-related brain inflammation. (C) 2015 Elsevier B.V. All rights reserved.
T2  - Behavioural Brain Research
T1  - The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-beta
VL  - 291
SP  - 130
EP  - 139
DO  - 10.1016/j.bbr.2015.05.029
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Brkić, Željka and Lukić, Iva and Radojčić, Marija",
year = "2015",
abstract = "Peripheral inflammation induced by lipopolysaccharide (LPS) causes behavioural changes indicative for depression. The possible mechanisms involve the interference with neuroinflammatory, neuroendocrine, and neurotrophic processes. Apart from heterogeneity in the molecular background, sexual context may be another factor relevant to the manifestation of mood disturbances upon an immune challenge. We investigated sex-dependent effects of a 7-day LPS treatment of adult Wistar rats on depressive-like behaviour and their relation with hypothalamic neuroendocrine factor, corticotrophin-releasing hormone (CRH), proplastic brain-derived neurotropic factor (BDNF), pro-inflammatory cyclooxygenase-2 (COX-2) and nuclear factor kappa beta (NFkB). Also, their regulators, the glucocorticoid receptor (GR) and CCAAT enhancer-binding protein (C/EBP) beta were followed. LPS induced depressive-like behaviour in females was associated with the increased hypothalamic CRH and decreased BDNF, but not with COX-2. These changes were paralleled by an increase in nuclear GR, NFkB and 20 kDa C/EBP beta. LPS also altered behaviour in males and increased CRH expression, but in contrast to females, this was accompanied with the elevated COX-2, accumulation of cytosolic GR and elevated nuclear 38 kDa C/EBP beta and NFkB. In conclusion, depressive-like phenotype induced by LPS in both sexes emerges from similar HPA axis activation and sex-specific alterations of hypothalamic molecular signalling: in males it is related to compromised control of neuroinflamation connected with cytoplasmic GR retention, while in females it is related to diminished proplastic capacity of BDNF. Sex-dependent mechanisms by which inflammation alters hypothalamic processes and cause pathological behaviour in animals, could be operative in the treatment of depression-related brain inflammation. (C) 2015 Elsevier B.V. All rights reserved.",
journal = "Behavioural Brain Research",
title = "The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-beta",
volume = "291",
pages = "130-139",
doi = "10.1016/j.bbr.2015.05.029"
}

Adžić, M., Đorđević, J. D., Mitić, M., Brkić, Ž., Lukić, I.,& Radojčić, M.. (2015). The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-beta. in Behavioural Brain Research, 291, 130-139.
https://doi.org/10.1016/j.bbr.2015.05.029

Adžić M, Đorđević JD, Mitić M, Brkić Ž, Lukić I, Radojčić M. The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-beta. in Behavioural Brain Research. 2015;291:130-139.
doi:10.1016/j.bbr.2015.05.029 .

Adžić, Miroslav, Đorđević, Jelena D., Mitić, Miloš, Brkić, Željka, Lukić, Iva, Radojčić, Marija, "The contribution of hypothalamic neuroendocrine, neuroplastic and neuroinflammatory processes to lipopolysaccharide-induced depressive-like behaviour in female and male rats: Involvement of glucocorticoid receptor and C/EBP-beta" in Behavioural Brain Research, 291 (2015):130-139,
https://doi.org/10.1016/j.bbr.2015.05.029 . .

TY  - JOUR
AU  - Jovičić, Milica J.
AU  - Lukić, Iva
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
AU  - Marić, Nađa P.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/723
AB  - Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved.
T2  - Medical Hypotheses
T1  - Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression
VL  - 85
IS  - 3
SP  - 291
EP  - 294
DO  - 10.1016/j.mehy.2015.05.015
ER  - 

@article{
author = "Jovičić, Milica J. and Lukić, Iva and Radojčić, Marija and Adžić, Miroslav and Marić, Nađa P.",
year = "2015",
abstract = "Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved.",
journal = "Medical Hypotheses",
title = "Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression",
volume = "85",
number = "3",
pages = "291-294",
doi = "10.1016/j.mehy.2015.05.015"
}

Jovičić, M. J., Lukić, I., Radojčić, M., Adžić, M.,& Marić, N. P.. (2015). Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression. in Medical Hypotheses, 85(3), 291-294.
https://doi.org/10.1016/j.mehy.2015.05.015

Jovičić MJ, Lukić I, Radojčić M, Adžić M, Marić NP. Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression. in Medical Hypotheses. 2015;85(3):291-294.
doi:10.1016/j.mehy.2015.05.015 .

Jovičić, Milica J., Lukić, Iva, Radojčić, Marija, Adžić, Miroslav, Marić, Nađa P., "Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression" in Medical Hypotheses, 85, no. 3 (2015):291-294,
https://doi.org/10.1016/j.mehy.2015.05.015 . .

TY  - CHAP
AU  - Adžić, Miroslav
AU  - Mitić, Miloš
AU  - Lukić, Iva
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija B.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10585
AB  - Major depression is a very common and serious mood disorder characterized by heterogeneous etiopathology. Treatment of the disease usually involves the use of antidepressant medications whose basic mechanism is achieved via increasing synaptic levels of monoamine neurotransmitters in different brain regions affected by the disease. Currently used antidepressant medications display limited efficacy with a pronounced delay to onset of action, and they all provoke disturbing side effects. With the ultimate goal of uncovering the primary postsynaptic actions that may initiate cellular antidepressive signaling, basic and clinical researches are devoted to studying the effects of antidepressants, particularly those most commonly used, selective serotonin reuptake inhibitors (SSRIs), on the complex signaling network that is known to be altered in depression. This includes the effects of antidepressants on the hypothalamic-pituitaryadrenal axis (HPA) activity, production of neurotrophins and regulation of neurogenesis, pro-inflammatory and anti-inflammatory cytokines, oxidative stress and mitochondrial functioning. Herein, we discuss the latest published data from animal and clinical studies that have examined the effects of different SSRIs on depression-related pathophysiological mechanisms. Special attention will be dedicated to gender-specific effects of SSRIs action and to their adverse effects. © 2015 by Nova Science Publishers, Inc. All rights reserved.
T2  - Fluoxetine: Pharmacology, Mechanisms of Action and Potential Side Effects
T1  - Role of fluoxetine on depression-related pathophysiological mechanisms
SP  - 227
EP  - 278
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10585
ER  - 

@inbook{
author = "Adžić, Miroslav and Mitić, Miloš and Lukić, Iva and Đorđević, Jelena D. and Radojčić, Marija B.",
year = "2015",
abstract = "Major depression is a very common and serious mood disorder characterized by heterogeneous etiopathology. Treatment of the disease usually involves the use of antidepressant medications whose basic mechanism is achieved via increasing synaptic levels of monoamine neurotransmitters in different brain regions affected by the disease. Currently used antidepressant medications display limited efficacy with a pronounced delay to onset of action, and they all provoke disturbing side effects. With the ultimate goal of uncovering the primary postsynaptic actions that may initiate cellular antidepressive signaling, basic and clinical researches are devoted to studying the effects of antidepressants, particularly those most commonly used, selective serotonin reuptake inhibitors (SSRIs), on the complex signaling network that is known to be altered in depression. This includes the effects of antidepressants on the hypothalamic-pituitaryadrenal axis (HPA) activity, production of neurotrophins and regulation of neurogenesis, pro-inflammatory and anti-inflammatory cytokines, oxidative stress and mitochondrial functioning. Herein, we discuss the latest published data from animal and clinical studies that have examined the effects of different SSRIs on depression-related pathophysiological mechanisms. Special attention will be dedicated to gender-specific effects of SSRIs action and to their adverse effects. © 2015 by Nova Science Publishers, Inc. All rights reserved.",
journal = "Fluoxetine: Pharmacology, Mechanisms of Action and Potential Side Effects",
booktitle = "Role of fluoxetine on depression-related pathophysiological mechanisms",
pages = "227-278",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10585"
}

Adžić, M., Mitić, M., Lukić, I., Đorđević, J. D.,& Radojčić, M. B.. (2015). Role of fluoxetine on depression-related pathophysiological mechanisms. in Fluoxetine: Pharmacology, Mechanisms of Action and Potential Side Effects, 227-278.
https://hdl.handle.net/21.15107/rcub_vinar_10585

Adžić M, Mitić M, Lukić I, Đorđević JD, Radojčić MB. Role of fluoxetine on depression-related pathophysiological mechanisms. in Fluoxetine: Pharmacology, Mechanisms of Action and Potential Side Effects. 2015;:227-278.
https://hdl.handle.net/21.15107/rcub_vinar_10585 .

Adžić, Miroslav, Mitić, Miloš, Lukić, Iva, Đorđević, Jelena D., Radojčić, Marija B., "Role of fluoxetine on depression-related pathophysiological mechanisms" in Fluoxetine: Pharmacology, Mechanisms of Action and Potential Side Effects (2015):227-278,
https://hdl.handle.net/21.15107/rcub_vinar_10585 .

TY  - JOUR
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Tatalović, Nikola R.
AU  - Božović, Natalija
AU  - Soldatovic, Ivan
AU  - Mihaljević, Marina
AU  - Pavlović, Zorana
AU  - Radojčić, Marija
AU  - Marić, Nađa P.
AU  - Adžić, Miroslav
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/148
AB  - Background: Oxidative stress is reliably observed in major depressive disorder (MDD). However, molecular data on the principal cellular redox-sensitive transcriptional factors and the levels of their downstream-regulated antioxidant enzymes in MDD are scarce. Methods: In the peripheral blood mononuclear cells (PBMC) of subjects with a current episode of MDD (n = 30) and healthy controls (n = 35), we investigated alterations in the levels of redox-sensing nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein, its inhibitor Keap1, and nuclear factor-kappa B (NF-kappa B), along with their cognate downstream effectors, the antioxidant enzymes (AOEs): manganese and copper zinc superoxide dismutase (MnSOD and CuZnSOD, respectively), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR). Results: MDD subjects exhibited higher levels of Nrf2 and its regulator Keap1, as well as NF-kappa B in the cytoplasm of PBMC compared to controls. This state was further reflected by increased levels of MnSOD, CuZnSOD and CAT proteins and by the lack of correlation between MnSOD and CAT, which could indicate impaired oxidative detoxification capacity in MDD patients. Moreover, increased levels of MnSOD, CuZnSOD and CAT in MDD patients positively correlated with levels of Nrf2, while increased levels of SODs were also positively related to NF-kappa B. There were no differences regarding the levels of GPx and GLR proteins, but the ratio of GLR/GPx was reduced, suggesting diminished capacity of GPx in antioxidative defence in PBMC of MDD subjects. Conclusion: These data provide evidence that MDD is characterized by up-regulation of redox-sensitive transcriptional factors (Nrf2 and NF-kappa B) and AOEs (MnSOD, CuZnSOD and CAT), indicating pro-oxidative state in the PBMC of MDD patients. (C) 2014 S. Karger AG, Basel
T2  - Neuropsychobiology
T1  - Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive Patients
VL  - 70
IS  - 1
SP  - 1
EP  - 9
DO  - 10.1159/000362841
ER  - 

@article{
author = "Lukić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Tatalović, Nikola R. and Božović, Natalija and Soldatovic, Ivan and Mihaljević, Marina and Pavlović, Zorana and Radojčić, Marija and Marić, Nađa P. and Adžić, Miroslav",
year = "2014",
abstract = "Background: Oxidative stress is reliably observed in major depressive disorder (MDD). However, molecular data on the principal cellular redox-sensitive transcriptional factors and the levels of their downstream-regulated antioxidant enzymes in MDD are scarce. Methods: In the peripheral blood mononuclear cells (PBMC) of subjects with a current episode of MDD (n = 30) and healthy controls (n = 35), we investigated alterations in the levels of redox-sensing nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protein, its inhibitor Keap1, and nuclear factor-kappa B (NF-kappa B), along with their cognate downstream effectors, the antioxidant enzymes (AOEs): manganese and copper zinc superoxide dismutase (MnSOD and CuZnSOD, respectively), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR). Results: MDD subjects exhibited higher levels of Nrf2 and its regulator Keap1, as well as NF-kappa B in the cytoplasm of PBMC compared to controls. This state was further reflected by increased levels of MnSOD, CuZnSOD and CAT proteins and by the lack of correlation between MnSOD and CAT, which could indicate impaired oxidative detoxification capacity in MDD patients. Moreover, increased levels of MnSOD, CuZnSOD and CAT in MDD patients positively correlated with levels of Nrf2, while increased levels of SODs were also positively related to NF-kappa B. There were no differences regarding the levels of GPx and GLR proteins, but the ratio of GLR/GPx was reduced, suggesting diminished capacity of GPx in antioxidative defence in PBMC of MDD subjects. Conclusion: These data provide evidence that MDD is characterized by up-regulation of redox-sensitive transcriptional factors (Nrf2 and NF-kappa B) and AOEs (MnSOD, CuZnSOD and CAT), indicating pro-oxidative state in the PBMC of MDD patients. (C) 2014 S. Karger AG, Basel",
journal = "Neuropsychobiology",
title = "Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive Patients",
volume = "70",
number = "1",
pages = "1-9",
doi = "10.1159/000362841"
}

Lukić, I., Mitić, M., Đorđević, J. D., Tatalović, N. R., Božović, N., Soldatovic, I., Mihaljević, M., Pavlović, Z., Radojčić, M., Marić, N. P.,& Adžić, M.. (2014). Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive Patients. in Neuropsychobiology, 70(1), 1-9.
https://doi.org/10.1159/000362841

Lukić I, Mitić M, Đorđević JD, Tatalović NR, Božović N, Soldatovic I, Mihaljević M, Pavlović Z, Radojčić M, Marić NP, Adžić M. Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive Patients. in Neuropsychobiology. 2014;70(1):1-9.
doi:10.1159/000362841 .

Lukić, Iva, Mitić, Miloš, Đorđević, Jelena D., Tatalović, Nikola R., Božović, Natalija, Soldatovic, Ivan, Mihaljević, Marina, Pavlović, Zorana, Radojčić, Marija, Marić, Nađa P., Adžić, Miroslav, "Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive Patients" in Neuropsychobiology, 70, no. 1 (2014):1-9,
https://doi.org/10.1159/000362841 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Lukić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Krstić-Demonacos, Marija
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5868
AB  - Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Psychoneuroendocrinology
T1  - Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism
VL  - 38
IS  - 12
SP  - 2914
EP  - 2924
DO  - 10.1016/j.psyneuen.2013.07.019
ER  - 

@article{
author = "Adžić, Miroslav and Lukić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Elaković, Ivana and Đorđević, Ana D. and Krstić-Demonacos, Marija and Matić, Gordana and Radojčić, Marija",
year = "2013",
abstract = "Antidepressants affect glucocorticoid receptor (GR) functioning partly through modulation of its phosphorylation but their effects on mitochondrial GR have remained undefined. We investigated the ability of chronic fiuoxetine treatment to affect chronic stress-induced changes of mitochondrial GR and its phosphoisoforms (pGRs) in the prefrontal cortex and hippocampus of female and male rats. Since mitochondrial GR regulates oxidative phosphorylation, expression of mitochondrial-encoded subunits of cytochrome (cyt) c oxidase and its activity were also investigated. Chronic stress caused accumulation of the GR in mitochondria of female prefrontal cortex, while the changes in the hippocampus were sex-specific at the levels of pGRs. Expression of mitochondrial COXs genes corresponded to chronic stress-modulated mitochondrial GR in both tissues of both genders and to cyt c oxidase activity in females. Moreover, the metabolic parameters in stressed animals were affected by fiuoxetine therapy only in the hippocampus. Namely, fluoxetine effects on mitochondrial COXs and cyt c oxidase activity in the hippocampus seem to be conveyed through pGR232 in females, while in males this likely occurs through other mechanisms. In summary, sex-specific regulation of cyt c oxidase by the stress and antidepressant treatment and its differential convergence with mitochondrial GR signaling in the prefrontal cortex and hippocampus could contribute to clarification of sex-dependent vulnerability to stress-related disorders and sex-specific clinical impact of antidepressants. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Psychoneuroendocrinology",
title = "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism",
volume = "38",
number = "12",
pages = "2914-2924",
doi = "10.1016/j.psyneuen.2013.07.019"
}

Adžić, M., Lukić, I., Mitić, M., Đorđević, J. D., Elaković, I., Đorđević, A. D., Krstić-Demonacos, M., Matić, G.,& Radojčić, M.. (2013). Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology, 38(12), 2914-2924.
https://doi.org/10.1016/j.psyneuen.2013.07.019

Adžić M, Lukić I, Mitić M, Đorđević JD, Elaković I, Đorđević AD, Krstić-Demonacos M, Matić G, Radojčić M. Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism. in Psychoneuroendocrinology. 2013;38(12):2914-2924.
doi:10.1016/j.psyneuen.2013.07.019 .

Adžić, Miroslav, Lukić, Iva, Mitić, Miloš, Đorđević, Jelena D., Elaković, Ivana, Đorđević, Ana D., Krstić-Demonacos, Marija, Matić, Gordana, Radojčić, Marija, "Brain region- and sex-specific modulation of mitochondrial glucocorticoid receptor phosphorylation in fluoxetine treated stressed rats: Effects on energy metabolism" in Psychoneuroendocrinology, 38, no. 12 (2013):2914-2924,
https://doi.org/10.1016/j.psyneuen.2013.07.019 . .

TY  - CONF
AU  - Marić, N. P.
AU  - Simić, Iva
AU  - Pavlović, Z.
AU  - Mitić, Miloš
AU  - Soldatović, I.
AU  - Andrić, S.
AU  - Mihaljević, M.
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5988
C3  - European Psychiatry
T1  - Phosphorylation of Peripheral Glucocorticoid Receptor in the Continuum from Current Depressive Episode to Vulnerability to Depression
VL  - 28
UR  - https://hdl.handle.net/21.15107/rcub_vinar_5988
ER  - 

@conference{
author = "Marić, N. P. and Simić, Iva and Pavlović, Z. and Mitić, Miloš and Soldatović, I. and Andrić, S. and Mihaljević, M. and Radojčić, Marija and Adžić, Miroslav",
year = "2013",
journal = "European Psychiatry",
title = "Phosphorylation of Peripheral Glucocorticoid Receptor in the Continuum from Current Depressive Episode to Vulnerability to Depression",
volume = "28",
url = "https://hdl.handle.net/21.15107/rcub_vinar_5988"
}

Marić, N. P., Simić, I., Pavlović, Z., Mitić, M., Soldatović, I., Andrić, S., Mihaljević, M., Radojčić, M.,& Adžić, M.. (2013). Phosphorylation of Peripheral Glucocorticoid Receptor in the Continuum from Current Depressive Episode to Vulnerability to Depression. in European Psychiatry, 28.
https://hdl.handle.net/21.15107/rcub_vinar_5988

Marić NP, Simić I, Pavlović Z, Mitić M, Soldatović I, Andrić S, Mihaljević M, Radojčić M, Adžić M. Phosphorylation of Peripheral Glucocorticoid Receptor in the Continuum from Current Depressive Episode to Vulnerability to Depression. in European Psychiatry. 2013;28.
https://hdl.handle.net/21.15107/rcub_vinar_5988 .

Marić, N. P., Simić, Iva, Pavlović, Z., Mitić, Miloš, Soldatović, I., Andrić, S., Mihaljević, M., Radojčić, Marija, Adžić, Miroslav, "Phosphorylation of Peripheral Glucocorticoid Receptor in the Continuum from Current Depressive Episode to Vulnerability to Depression" in European Psychiatry, 28 (2013),
https://hdl.handle.net/21.15107/rcub_vinar_5988 .

TY  - JOUR
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Đorđević, Jelena D.
AU  - Adžić, Miroslav
AU  - Radojčić, Marija
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5523
AB  - Chronic psychosocial isolation stress (CPSI) modulates glucocorticoid receptor (GR) functioning in Wistar male rat hippocampus (HIPPO) through alteration of nuclear GR phosphorylation and its upstream kinases signaling, which parallels animal depressive-like behavior. The current study investigated potential gender specificities regarding the effect of chronic therapy by an antidepressant fluoxetine (FLU) on GR signaling in HIPPO and depressive-like behavior in CPSI animals. FLU was administrated to female and male naive or CPSI rats for 21 days and GR protein, its phosphorylation status and upstream kinases, as well as GR and BDNF mRNA were followed in HIPPO together with animal serum corticosterone (CORT) and depressive-like behavior. The results showed that CPSI increased immobility in males versus hyperactivity in females and disrupted nuclear pGR232-Cdk5 pathway and JNK signaling in a gender-specific way. In contrast, in both genders CPSI increased the nuclear levels of GR and pGR246 but decreased CORT and mRNA levels of GR and BDNF. Concomitant FLU normalized the depressive-like behavior and altered the nuclear pGR232-Cdk5 signaling in a gender-specific manner. In both females and males, FLU reversed the nuclear levels of GR and pGR246 without affecting CORT and GR mRNA levels. In contrast, FLU exhibited gender-specific effect on BDNF mRNA in CPSI animals, by increasing it in females, but not in males. In spite of normalization the total nuclear GR level upon FLU treatment in both gender, down-regulation of GR mRNA is possibly maintained through prevalence of pGR232 isoform only in males. The gender-specific alterations of pGR232-Cdk5 signaling and BDNF gene expression in HIPPO and normalization of depressive-like behavior upon FLU treatment distinguishes this signaling pathway as potential future antidepressant target for gender-specific therapy of stress related mood disorders. (C) 2013 Elsevier Ltd. All rights reserved.
T2  - Neuropharmacology
T1  - Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats
VL  - 70
SP  - 100
EP  - 111
DO  - 10.1016/j.neuropharm.2012.12.012
ER  - 

@article{
author = "Mitić, Miloš and Simić, Iva and Đorđević, Jelena D. and Adžić, Miroslav and Radojčić, Marija",
year = "2013",
abstract = "Chronic psychosocial isolation stress (CPSI) modulates glucocorticoid receptor (GR) functioning in Wistar male rat hippocampus (HIPPO) through alteration of nuclear GR phosphorylation and its upstream kinases signaling, which parallels animal depressive-like behavior. The current study investigated potential gender specificities regarding the effect of chronic therapy by an antidepressant fluoxetine (FLU) on GR signaling in HIPPO and depressive-like behavior in CPSI animals. FLU was administrated to female and male naive or CPSI rats for 21 days and GR protein, its phosphorylation status and upstream kinases, as well as GR and BDNF mRNA were followed in HIPPO together with animal serum corticosterone (CORT) and depressive-like behavior. The results showed that CPSI increased immobility in males versus hyperactivity in females and disrupted nuclear pGR232-Cdk5 pathway and JNK signaling in a gender-specific way. In contrast, in both genders CPSI increased the nuclear levels of GR and pGR246 but decreased CORT and mRNA levels of GR and BDNF. Concomitant FLU normalized the depressive-like behavior and altered the nuclear pGR232-Cdk5 signaling in a gender-specific manner. In both females and males, FLU reversed the nuclear levels of GR and pGR246 without affecting CORT and GR mRNA levels. In contrast, FLU exhibited gender-specific effect on BDNF mRNA in CPSI animals, by increasing it in females, but not in males. In spite of normalization the total nuclear GR level upon FLU treatment in both gender, down-regulation of GR mRNA is possibly maintained through prevalence of pGR232 isoform only in males. The gender-specific alterations of pGR232-Cdk5 signaling and BDNF gene expression in HIPPO and normalization of depressive-like behavior upon FLU treatment distinguishes this signaling pathway as potential future antidepressant target for gender-specific therapy of stress related mood disorders. (C) 2013 Elsevier Ltd. All rights reserved.",
journal = "Neuropharmacology",
title = "Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats",
volume = "70",
pages = "100-111",
doi = "10.1016/j.neuropharm.2012.12.012"
}

Mitić, M., Simić, I., Đorđević, J. D., Adžić, M.,& Radojčić, M.. (2013). Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats. in Neuropharmacology, 70, 100-111.
https://doi.org/10.1016/j.neuropharm.2012.12.012

Mitić M, Simić I, Đorđević JD, Adžić M, Radojčić M. Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats. in Neuropharmacology. 2013;70:100-111.
doi:10.1016/j.neuropharm.2012.12.012 .

Mitić, Miloš, Simić, Iva, Đorđević, Jelena D., Adžić, Miroslav, Radojčić, Marija, "Gender-specific effects of fluoxetine on hippocampal glucocorticoid receptor phosphorylation and behavior in chronically stressed rats" in Neuropharmacology, 70 (2013):100-111,
https://doi.org/10.1016/j.neuropharm.2012.12.012 . .

TY  - JOUR
AU  - Aleksić, Obrad S.
AU  - Nikolić, M. V.
AU  - Luković, Miloljub D.
AU  - Nikolic, N.
AU  - Radojčić, Marija
AU  - Radovanovic, M.
AU  - Đurić, Zorica
AU  - Mitrić, Miodrag
AU  - Nikolic, P. M.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4366
AB  - A simple ball milling/thermal treatment procedure was applied to obtain fine thermistor powders. Three different powder compositions were analyzed-Cu0.2Ni0.5Zn1.0Mn1.3O4, Cu0.25Ni0.5Zn1.0Mn1.25O4 and Cu0.4Ni0.5Mn2.1O4. XRD analysis showed that all three powder compositions had a cubic spinel structure. Correlation between the sintering temperature, structure and resulting electrical properties was analyzed on bulk samples. Thick film pastes were composed and segmented thick film thermistors were screen printed on alumina, dried and fired. SEM analysis revealed a typical dendrite structure with small grains and a developed surface area. Thick film sheet resistance was measured on a test matrix and the resistance decreased with increasing Cu content. The temperature dependence of sample resistance was measured in a climatic chamber enabling calculation of the material constant and activation energy. Aging of the obtained segmented thermistors was analyzed and the resistivity drift was 0.23% for the Cu0.2Ni0.5Zn1.0Mn1.3O4 NTC thick film thermistor confirming greater stability of thermistors containing Zn and Cu that in combination with the determined good thermistor characteristics make them good candidates for temperature and heat loss sensor applications. (C) 2012 Elsevier B.V. All rights reserved.
T2  - Materials Science and Engineering. B: Advanced Functional Solid-State Materials
T1  - Preparation and characterization of Cu and Zn modified nickel manganite NTC powders and thick film thermistors
VL  - 178
IS  - 3
SP  - 202
EP  - 210
DO  - 10.1016/j.mseb.2012.11.003
ER  - 

@article{
author = "Aleksić, Obrad S. and Nikolić, M. V. and Luković, Miloljub D. and Nikolic, N. and Radojčić, Marija and Radovanovic, M. and Đurić, Zorica and Mitrić, Miodrag and Nikolic, P. M.",
year = "2013",
abstract = "A simple ball milling/thermal treatment procedure was applied to obtain fine thermistor powders. Three different powder compositions were analyzed-Cu0.2Ni0.5Zn1.0Mn1.3O4, Cu0.25Ni0.5Zn1.0Mn1.25O4 and Cu0.4Ni0.5Mn2.1O4. XRD analysis showed that all three powder compositions had a cubic spinel structure. Correlation between the sintering temperature, structure and resulting electrical properties was analyzed on bulk samples. Thick film pastes were composed and segmented thick film thermistors were screen printed on alumina, dried and fired. SEM analysis revealed a typical dendrite structure with small grains and a developed surface area. Thick film sheet resistance was measured on a test matrix and the resistance decreased with increasing Cu content. The temperature dependence of sample resistance was measured in a climatic chamber enabling calculation of the material constant and activation energy. Aging of the obtained segmented thermistors was analyzed and the resistivity drift was 0.23% for the Cu0.2Ni0.5Zn1.0Mn1.3O4 NTC thick film thermistor confirming greater stability of thermistors containing Zn and Cu that in combination with the determined good thermistor characteristics make them good candidates for temperature and heat loss sensor applications. (C) 2012 Elsevier B.V. All rights reserved.",
journal = "Materials Science and Engineering. B: Advanced Functional Solid-State Materials",
title = "Preparation and characterization of Cu and Zn modified nickel manganite NTC powders and thick film thermistors",
volume = "178",
number = "3",
pages = "202-210",
doi = "10.1016/j.mseb.2012.11.003"
}

Aleksić, O. S., Nikolić, M. V., Luković, M. D., Nikolic, N., Radojčić, M., Radovanovic, M., Đurić, Z., Mitrić, M.,& Nikolic, P. M.. (2013). Preparation and characterization of Cu and Zn modified nickel manganite NTC powders and thick film thermistors. in Materials Science and Engineering. B: Advanced Functional Solid-State Materials, 178(3), 202-210.
https://doi.org/10.1016/j.mseb.2012.11.003

Aleksić OS, Nikolić MV, Luković MD, Nikolic N, Radojčić M, Radovanovic M, Đurić Z, Mitrić M, Nikolic PM. Preparation and characterization of Cu and Zn modified nickel manganite NTC powders and thick film thermistors. in Materials Science and Engineering. B: Advanced Functional Solid-State Materials. 2013;178(3):202-210.
doi:10.1016/j.mseb.2012.11.003 .

Aleksić, Obrad S., Nikolić, M. V., Luković, Miloljub D., Nikolic, N., Radojčić, Marija, Radovanovic, M., Đurić, Zorica, Mitrić, Miodrag, Nikolic, P. M., "Preparation and characterization of Cu and Zn modified nickel manganite NTC powders and thick film thermistors" in Materials Science and Engineering. B: Advanced Functional Solid-State Materials, 178, no. 3 (2013):202-210,
https://doi.org/10.1016/j.mseb.2012.11.003 . .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4995
AB  - Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel
T2  - Neuropsychobiology
T1  - Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers
VL  - 66
IS  - 2
SP  - 112
EP  - 119
DO  - 10.1159/000338605
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Radojčić, Marija",
year = "2012",
abstract = "Chronic stress is a contributing risk factor in the development of psychiatric illnesses, including depressive disorders. The mechanisms of their psychopathology are multifaceted and include, besides others, alterations in the brain plasticity. Previously, we investigated the effects of chronic social stress in the limbic brain structures of Wistar rats (hippocampus, HIPPO, and prefrontal cortex, PFC) and found multiple characteristics that resembled alterations described in some clinical studies of depression. We extended our investigations and followed the behavior of stressed animals by the open field test (OFT) and forced swimming test (FST), and the expression and polysialylation of synaptic plasticity markers, neural cell adhesion molecule (NCAM) and L1, in the HIPPO and PFC. We also determined the adrenal gland mass and plasma corticosterone (CORT) as a terminal part of the hypothalamic-pituitary-adrenal axis activity. Our data indicated that stressed animals avoided the central zone in the OFT and displayed decreased swimming, but prolonged immobility in the FST. The animals exhibited marked hypertrophy of the adrenal gland cortex, in spite of decreased serum CORT. Simultaneously, the stressed animals exhibited an increase in NCAM mRNA expression in the HIPPO, but not in the PFC. The synaptosomal NCAM of the HIPPO was markedly polysialylated, while cortical PSA-NCAM was significantly decreased. The results showed that chronic social isolation of Wistar rats causes both anxiety-like and depression-like behavior. These alterations are parallel with molecular changes in the limbic brain, including diminished NCAM sialylation in the PFC. Together with our previous results, the current observations suggest that a chronic social isolation model may potentially be used to study molecular mechanisms that underlie depressive symptomatology. Copyright (c) 2012 S. Karger AG, Basel",
journal = "Neuropsychobiology",
title = "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers",
volume = "66",
number = "2",
pages = "112-119",
doi = "10.1159/000338605"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M.,& Radojčić, M.. (2012). Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers. in Neuropsychobiology, 66(2), 112-119.
https://doi.org/10.1159/000338605

Đorđević JD, Đorđević AD, Adžić M, Radojčić M. Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers. in Neuropsychobiology. 2012;66(2):112-119.
doi:10.1159/000338605 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Radojčić, Marija, "Effects of Chronic Social Isolation on Wistar Rat Behavior and Brain Plasticity Markers" in Neuropsychobiology, 66, no. 2 (2012):112-119,
https://doi.org/10.1159/000338605 . .

TY  - JOUR
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena D.
AU  - Elaković, Ivana
AU  - Adžić, Miroslav
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5042
AB  - The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex
VL  - 693
IS  - 1-3
SP  - 37
EP  - 44
DO  - 10.1016/j.ejphar.2012.07.042
ER  - 

@article{
author = "Đorđević, Ana D. and Đorđević, Jelena D. and Elaković, Ivana and Adžić, Miroslav and Matić, Gordana and Radojčić, Marija",
year = "2012",
abstract = "The prefrontal cortex is the brain region sensitive to detrimental effects of stress and even mild stress can rapidly impair its function. Aside from initiating proadaptive neuroplastic changes in the prefrontal cortex, chronic stress may also increase vulnerability of cortical neurons to apoptosis. Understanding the mechanism of plasticity and apoptotic processes is of immense importance for therapy of stress-related psychiatric disorders. In this study we tested whether molecular alterations in the prefrontal cortex, which occurred upon chronic social isolation, could be influenced by a prolonged fluoxetine treatment. We analyzed the expression of synaptic plasticity and apoptotic molecular markers in the prefrontal cortex of young-adult male Wistar rats exposed to 6-week social isolation with and without fluoxetine treatment during the last 3 weeks. Compartmental redistribution of NF kappa B transcription factor, involved in regulation of plasticity and apoptosis, was also examined. The level of synaptosomal polysialic neural cell adhesion molecule(PSA-NCAM) was increased in the prefrontal cortex of isolated rats as compared to untreated controls. Treatment with fluoxetine reduced the PSA-NCAM level only in isolated animals. In addition, mitochondrial Bax protein was elevated by chronic social isolation, while fluoxetine failed to abolish this effect. Inspite of elevated Bcl-2 in the mitochondria, the calculated Bax/Bcl-2 ratio and concomitant absence of NF kappa B activation pointed to initiation of apoptotic signaling in the prefrontal cortex. The result simply that fluoxetine influences plasticity in the prefrontal cortex of chronically isolated rats and fails to prevent stress-induced initiation of apoptosis in this brain structure. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex",
volume = "693",
number = "1-3",
pages = "37-44",
doi = "10.1016/j.ejphar.2012.07.042"
}

Đorđević, A. D., Đorđević, J. D., Elaković, I., Adžić, M., Matić, G.,& Radojčić, M.. (2012). Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology, 693(1-3), 37-44.
https://doi.org/10.1016/j.ejphar.2012.07.042

Đorđević AD, Đorđević JD, Elaković I, Adžić M, Matić G, Radojčić M. Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex. in European Journal of Pharmacology. 2012;693(1-3):37-44.
doi:10.1016/j.ejphar.2012.07.042 .

Đorđević, Ana D., Đorđević, Jelena D., Elaković, Ivana, Adžić, Miroslav, Matić, Gordana, Radojčić, Marija, "Effects of fluoxetine on plasticity and apoptosis evoked by chronic stress in rat prefrontal cortex" in European Journal of Pharmacology, 693, no. 1-3 (2012):37-44,
https://doi.org/10.1016/j.ejphar.2012.07.042 . .

TY  - CONF
AU  - Maric, N. P.
AU  - Simić, Iva
AU  - Adžić, Miroslav
AU  - Savić, Danka A.
AU  - Đorđević, Jelena D.
AU  - Mihaljevic, M.
AU  - Mitić, Miloš
AU  - Pavlović, Z.
AU  - Soldatovic, I.
AU  - Krstić-Demonacos, Marija
AU  - Jasovic-Gasic, M.
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4969
C3  - European Psychiatry
T1  - Phosphorylation of Leukocyte Glucocorticoid Receptor as a Measure of Stress Vulnerability in Healthy Women and Men
VL  - 27
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4969
ER  - 

@conference{
author = "Maric, N. P. and Simić, Iva and Adžić, Miroslav and Savić, Danka A. and Đorđević, Jelena D. and Mihaljevic, M. and Mitić, Miloš and Pavlović, Z. and Soldatovic, I. and Krstić-Demonacos, Marija and Jasovic-Gasic, M. and Radojčić, Marija",
year = "2012",
journal = "European Psychiatry",
title = "Phosphorylation of Leukocyte Glucocorticoid Receptor as a Measure of Stress Vulnerability in Healthy Women and Men",
volume = "27",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4969"
}

Maric, N. P., Simić, I., Adžić, M., Savić, D. A., Đorđević, J. D., Mihaljevic, M., Mitić, M., Pavlović, Z., Soldatovic, I., Krstić-Demonacos, M., Jasovic-Gasic, M.,& Radojčić, M.. (2012). Phosphorylation of Leukocyte Glucocorticoid Receptor as a Measure of Stress Vulnerability in Healthy Women and Men. in European Psychiatry, 27.
https://hdl.handle.net/21.15107/rcub_vinar_4969

Maric NP, Simić I, Adžić M, Savić DA, Đorđević JD, Mihaljevic M, Mitić M, Pavlović Z, Soldatovic I, Krstić-Demonacos M, Jasovic-Gasic M, Radojčić M. Phosphorylation of Leukocyte Glucocorticoid Receptor as a Measure of Stress Vulnerability in Healthy Women and Men. in European Psychiatry. 2012;27.
https://hdl.handle.net/21.15107/rcub_vinar_4969 .

Maric, N. P., Simić, Iva, Adžić, Miroslav, Savić, Danka A., Đorđević, Jelena D., Mihaljevic, M., Mitić, Miloš, Pavlović, Z., Soldatovic, I., Krstić-Demonacos, Marija, Jasovic-Gasic, M., Radojčić, Marija, "Phosphorylation of Leukocyte Glucocorticoid Receptor as a Measure of Stress Vulnerability in Healthy Women and Men" in European Psychiatry, 27 (2012),
https://hdl.handle.net/21.15107/rcub_vinar_4969 .

TY  - JOUR
AU  - Simić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4825
AB  - Chronic psychosocial isolation (CPSI) is known to cause several maladaptive changes in the limbic brain structures, which regulate the hypothalamic-pituitary-adrenal (HPA) axis activity. In this study, we focused our investigation on CPSI effects in the hypothalamus (HT) since it is a major driver of HPA axis activity. We also investigated whether the exposure to CPSI could alter the response to subsequent acute stress (30-min immobilization). In the HT, we followed cytosolic and nuclear levels of the glucocorticoid receptor (GR), as a mediator of HPA axis feedback inhibition, and its chaperones, the heat shock proteins (HSPs), hsp70 and hsp90. The CPSI did not cause any changes in either GR or HSPs levels. However, we observed increase of the GR and hsp70 in both HT cellular compartments as a response of na LT ve rats to acute stress, whereas the response of CPSI rats to acute stress was associated with elevation of the GR in the cytosol and decrease of HSPs in the nucleus. Thus, our data indicated reduced availability of HSPs to GR in both cytosol and nucleus of the HT under acute stress of CPSI animals, and therefore, pointed out to potentially negative effects of CPSI on GR function in the HT.
T2  - Cellular and Molecular Neurobiology
T1  - Chronic Stress Decreases Availability of Heat Shock Proteins to Glucocorticoid Receptor in Response to Novel Acute Stress in Wistar Rat Hypothalamus
VL  - 32
IS  - 4
SP  - 625
EP  - 632
DO  - 10.1007/s10571-012-9811-9
ER  - 

@article{
author = "Simić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Radojčić, Marija and Adžić, Miroslav",
year = "2012",
abstract = "Chronic psychosocial isolation (CPSI) is known to cause several maladaptive changes in the limbic brain structures, which regulate the hypothalamic-pituitary-adrenal (HPA) axis activity. In this study, we focused our investigation on CPSI effects in the hypothalamus (HT) since it is a major driver of HPA axis activity. We also investigated whether the exposure to CPSI could alter the response to subsequent acute stress (30-min immobilization). In the HT, we followed cytosolic and nuclear levels of the glucocorticoid receptor (GR), as a mediator of HPA axis feedback inhibition, and its chaperones, the heat shock proteins (HSPs), hsp70 and hsp90. The CPSI did not cause any changes in either GR or HSPs levels. However, we observed increase of the GR and hsp70 in both HT cellular compartments as a response of na LT ve rats to acute stress, whereas the response of CPSI rats to acute stress was associated with elevation of the GR in the cytosol and decrease of HSPs in the nucleus. Thus, our data indicated reduced availability of HSPs to GR in both cytosol and nucleus of the HT under acute stress of CPSI animals, and therefore, pointed out to potentially negative effects of CPSI on GR function in the HT.",
journal = "Cellular and Molecular Neurobiology",
title = "Chronic Stress Decreases Availability of Heat Shock Proteins to Glucocorticoid Receptor in Response to Novel Acute Stress in Wistar Rat Hypothalamus",
volume = "32",
number = "4",
pages = "625-632",
doi = "10.1007/s10571-012-9811-9"
}

Simić, I., Mitić, M., Đorđević, J. D., Radojčić, M.,& Adžić, M.. (2012). Chronic Stress Decreases Availability of Heat Shock Proteins to Glucocorticoid Receptor in Response to Novel Acute Stress in Wistar Rat Hypothalamus. in Cellular and Molecular Neurobiology, 32(4), 625-632.
https://doi.org/10.1007/s10571-012-9811-9

Simić I, Mitić M, Đorđević JD, Radojčić M, Adžić M. Chronic Stress Decreases Availability of Heat Shock Proteins to Glucocorticoid Receptor in Response to Novel Acute Stress in Wistar Rat Hypothalamus. in Cellular and Molecular Neurobiology. 2012;32(4):625-632.
doi:10.1007/s10571-012-9811-9 .

Simić, Iva, Mitić, Miloš, Đorđević, Jelena D., Radojčić, Marija, Adžić, Miroslav, "Chronic Stress Decreases Availability of Heat Shock Proteins to Glucocorticoid Receptor in Response to Novel Acute Stress in Wistar Rat Hypothalamus" in Cellular and Molecular Neurobiology, 32, no. 4 (2012):625-632,
https://doi.org/10.1007/s10571-012-9811-9 . .

TY  - CONF
AU  - Simić, Iva
AU  - Mitić, Miloš
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9291
AB  - Depression is one of the most pervasive and debilitating stress-related psychiatric
diseases worldwide. Cyclin-dependent kinase 5 (Cdk5) is of particular importance
for normal adult brain functioning and has recently been associated with anxiety
and depressive disorders. In the present study, we investigated how alterations in
depressive-like behavior are accompanied by the changes in hippocampal
Cdk5/p35/p25 signaling in female and male Wistar rats exposed to chronic
psychosocial isolation (CPSI) and concomitant antidepressant fluoxetine (FLU)
treatment. Our results showed that CPSI induced different behavioral responses in
female and male rats which were accompanied by dissimilarities in Cdk5/p35/p25
signaling. The effect of concomitant FLU treatment was also gender-specific
regarding behavioral responses and Cdk5 levels, but gender-independent regarding
p35 levels, which was accompanied with normalization of female and male rat
behavior.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
T1  - Chronic stress and concomitant fluoxetine treatment exert gender-specific effects on behavior and hippocampal Cd5 signaling in wistar rats
VL  - 1
SP  - 367
EP  - 369
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9291
ER  - 

@conference{
author = "Simić, Iva and Mitić, Miloš and Radojčić, Marija and Adžić, Miroslav",
year = "2012",
abstract = "Depression is one of the most pervasive and debilitating stress-related psychiatric
diseases worldwide. Cyclin-dependent kinase 5 (Cdk5) is of particular importance
for normal adult brain functioning and has recently been associated with anxiety
and depressive disorders. In the present study, we investigated how alterations in
depressive-like behavior are accompanied by the changes in hippocampal
Cdk5/p35/p25 signaling in female and male Wistar rats exposed to chronic
psychosocial isolation (CPSI) and concomitant antidepressant fluoxetine (FLU)
treatment. Our results showed that CPSI induced different behavioral responses in
female and male rats which were accompanied by dissimilarities in Cdk5/p35/p25
signaling. The effect of concomitant FLU treatment was also gender-specific
regarding behavioral responses and Cdk5 levels, but gender-independent regarding
p35 levels, which was accompanied with normalization of female and male rat
behavior.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry",
title = "Chronic stress and concomitant fluoxetine treatment exert gender-specific effects on behavior and hippocampal Cd5 signaling in wistar rats",
volume = "1",
pages = "367-369",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9291"
}

Simić, I., Mitić, M., Radojčić, M.,& Adžić, M.. (2012). Chronic stress and concomitant fluoxetine treatment exert gender-specific effects on behavior and hippocampal Cd5 signaling in wistar rats. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 1, 367-369.
https://hdl.handle.net/21.15107/rcub_vinar_9291

Simić I, Mitić M, Radojčić M, Adžić M. Chronic stress and concomitant fluoxetine treatment exert gender-specific effects on behavior and hippocampal Cd5 signaling in wistar rats. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry. 2012;1:367-369.
https://hdl.handle.net/21.15107/rcub_vinar_9291 .

Simić, Iva, Mitić, Miloš, Radojčić, Marija, Adžić, Miroslav, "Chronic stress and concomitant fluoxetine treatment exert gender-specific effects on behavior and hippocampal Cd5 signaling in wistar rats" in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry, 1 (2012):367-369,
https://hdl.handle.net/21.15107/rcub_vinar_9291 .

TY  - CONF
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9286
AB  - c-Jun N-terminal kinases (JNKs) are important stress-responsive kinases that act as
mediators in synaptic remodeling and neuronal degeneration in response to stress
and, thus receiving considerable attention as potential therapeutic targets. In the
present study, we investigated how exposure to chronic stress (chronic
psychosocial isolation, CPSI) and subsequent therapy with antidepressant
fluoxetine (FLU) affects the nuclear JNKs signalling and its phosphorylation status
in the hippocampus (HIPPO) of the female and male Wistar rats. Our results
showed that CPSI disrupted nuclear JNKs signaling in a gender specific way, while
concomitant FLU treatment normalized JNKs only in HIPPO of females.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
T1  - Antidepresant fluoxetine normalizes brain JNKs signaling impaired by chronic stress in female but not in male wistar rats
VL  - 1
VL  - 1
SP  - 364
EP  - 366
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9286
ER  - 

@conference{
author = "Mitić, Miloš and Simić, Iva and Radojčić, Marija and Adžić, Miroslav",
year = "2012",
abstract = "c-Jun N-terminal kinases (JNKs) are important stress-responsive kinases that act as
mediators in synaptic remodeling and neuronal degeneration in response to stress
and, thus receiving considerable attention as potential therapeutic targets. In the
present study, we investigated how exposure to chronic stress (chronic
psychosocial isolation, CPSI) and subsequent therapy with antidepressant
fluoxetine (FLU) affects the nuclear JNKs signalling and its phosphorylation status
in the hippocampus (HIPPO) of the female and male Wistar rats. Our results
showed that CPSI disrupted nuclear JNKs signaling in a gender specific way, while
concomitant FLU treatment normalized JNKs only in HIPPO of females.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry",
title = "Antidepresant fluoxetine normalizes brain JNKs signaling impaired by chronic stress in female but not in male wistar rats",
volume = "1, 1",
pages = "364-366",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9286"
}

Mitić, M., Simić, I., Radojčić, M.,& Adžić, M.. (2012). Antidepresant fluoxetine normalizes brain JNKs signaling impaired by chronic stress in female but not in male wistar rats. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 1, 364-366.
https://hdl.handle.net/21.15107/rcub_vinar_9286

Mitić M, Simić I, Radojčić M, Adžić M. Antidepresant fluoxetine normalizes brain JNKs signaling impaired by chronic stress in female but not in male wistar rats. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry. 2012;1:364-366.
https://hdl.handle.net/21.15107/rcub_vinar_9286 .

Mitić, Miloš, Simić, Iva, Radojčić, Marija, Adžić, Miroslav, "Antidepresant fluoxetine normalizes brain JNKs signaling impaired by chronic stress in female but not in male wistar rats" in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry, 1 (2012):364-366,
https://hdl.handle.net/21.15107/rcub_vinar_9286 .

TY  - CONF
AU  - Adžić, Miroslav
AU  - Simić, Iva
AU  - Mitić, Miloš
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9283
AB  - The activity of cytochrome c oxidase correlates with neuronal functional activity
and is considered as an ideal marker for examining the effects of antidepressant
treatment on brain metabolism. We investigated gender specific effects of
antidepressant fluoxetine on cytochrome c oxidase activity in the mitochondria of
prefrontal cortex (PFC) of chronically isolated female and male Wistar rats. Our
results showed that chronic psychosocial isolation (CPSI) increased cytochrome c
oxidase activity in female PFC, while in males, this activity was decreased.
Fluoxetine treatment did not normalize cytochrome c oxidase activity in either
CPSI females or CPSI males. Our data suggest that the pattern of PFC energy
metabolism impairment by CPSI is related to gender, but that fluoxetine treatment
was unable to ameliorate these defects.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
T1  - Chronic stress impairment of prefrontal cortex energy metabolism is related to gender and can not be ameliorated by antidepresant fluoxetine
VL  - 1
SP  - 361
EP  - 363
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9283
ER  - 

@conference{
author = "Adžić, Miroslav and Simić, Iva and Mitić, Miloš and Đorđević, Jelena D. and Radojčić, Marija",
year = "2012",
abstract = "The activity of cytochrome c oxidase correlates with neuronal functional activity
and is considered as an ideal marker for examining the effects of antidepressant
treatment on brain metabolism. We investigated gender specific effects of
antidepressant fluoxetine on cytochrome c oxidase activity in the mitochondria of
prefrontal cortex (PFC) of chronically isolated female and male Wistar rats. Our
results showed that chronic psychosocial isolation (CPSI) increased cytochrome c
oxidase activity in female PFC, while in males, this activity was decreased.
Fluoxetine treatment did not normalize cytochrome c oxidase activity in either
CPSI females or CPSI males. Our data suggest that the pattern of PFC energy
metabolism impairment by CPSI is related to gender, but that fluoxetine treatment
was unable to ameliorate these defects.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry",
title = "Chronic stress impairment of prefrontal cortex energy metabolism is related to gender and can not be ameliorated by antidepresant fluoxetine",
volume = "1",
pages = "361-363",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9283"
}

Adžić, M., Simić, I., Mitić, M., Đorđević, J. D.,& Radojčić, M.. (2012). Chronic stress impairment of prefrontal cortex energy metabolism is related to gender and can not be ameliorated by antidepresant fluoxetine. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 1, 361-363.
https://hdl.handle.net/21.15107/rcub_vinar_9283

Adžić M, Simić I, Mitić M, Đorđević JD, Radojčić M. Chronic stress impairment of prefrontal cortex energy metabolism is related to gender and can not be ameliorated by antidepresant fluoxetine. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry. 2012;1:361-363.
https://hdl.handle.net/21.15107/rcub_vinar_9283 .

Adžić, Miroslav, Simić, Iva, Mitić, Miloš, Đorđević, Jelena D., Radojčić, Marija, "Chronic stress impairment of prefrontal cortex energy metabolism is related to gender and can not be ameliorated by antidepresant fluoxetine" in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry, 1 (2012):361-363,
https://hdl.handle.net/21.15107/rcub_vinar_9283 .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4329
AB  - Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmacology
T1  - Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver
VL  - 659
IS  - 1
SP  - 61
EP  - 66
DO  - 10.1016/j.ejphar.2011.03.003
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Selective serotonin reuptake inhibitors (SSRI) are a treatment of choice for stress related disorders including clinical depression and a range of anxiety-related disorders. In the experimental animals, chronic stress paradigms are considered as a model of depression, and in that context are used for examining the effects of different drug treatments. The present research was designed to investigate the effect of SSRI fluoxetine on antioxidant status and apoptotic signaling in Wistar rat liver, which is a central organ for activation and detoxification of many xenobiotics and reactive oxygen species. We also investigated whether chronic fluoxetine treatment exhibits the same effects in the liver of control animals vs. animals stressed by chronic psychosocial isolation. Our results revealed that fluoxetine downregulated the activity of superoxide dismutases and upregulated the activity of glutathione peroxidase in both rat groups, while elevating glutathione reductase activity and total antioxidant status only in stressed animals. These results suggested that fluoxetine interfered with stress-induced pathways of oxidative defense in the liver. In addition, in both experimental groups, fluoxetine induced several hallmarks of apoptosis in the liver, including a decrease in Bcl-2 expression and increased DNA fragmentation. However, apoptotic alterations were more pronounced in stressed animals, suggesting that stress related oxidative damage could have primed apoptotic effects of fluoxetine. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmacology",
title = "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver",
volume = "659",
number = "1",
pages = "61-66",
doi = "10.1016/j.ejphar.2011.03.003"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology, 659(1), 61-66.
https://doi.org/10.1016/j.ejphar.2011.03.003

Đorđević JD, Đorđević AD, Adžić M, Elaković I, Matić G, Radojčić M. Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver. in European Journal of Pharmacology. 2011;659(1):61-66.
doi:10.1016/j.ejphar.2011.03.003 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver" in European Journal of Pharmacology, 659, no. 1 (2011):61-66,
https://doi.org/10.1016/j.ejphar.2011.03.003 . .

TY  - JOUR
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Rackov, Gorjana
AU  - Đorđević, Ana D.
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4640
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.
T2  - Acta Chimica Slovenica
T1  - Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats
VL  - 58
IS  - 4
SP  - 785
EP  - 791
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4640
ER  - 

@article{
author = "Adžić, Miroslav and Đorđević, Jelena D. and Mitić, Miloš and Simić, Iva and Rackov, Gorjana and Đorđević, Ana D. and Elaković, Ivana and Matić, Gordana and Radojčić, Marija",
year = "2011",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered critical for pathophysiology of stress related psychiatric disorders, and their status in blood serves as biomarker for effects of pharmacological treatments. The present study was designed to investigate the modulation of erythrocyte antioxidant enzymes (AOEs): CuZn superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR) activities and their protein expression in Wistar male rats subjected to chronic psychosocial isolation and/or to pharmacological treatment with fluoxetine. Chronically isolated animals exhibited decreased levels of serum corticosterone, as opposed to other chronic stress paradigms. In addition to that, SOD, CAT and GPx status was not altered either by chronic psychosocial isolation or by fluoxetine treatment. In contrast, GLR activity and its protein level were both markedly reduced by fluoxetine. Since, GLR is crucial for overall oxido-reductive balance through maintaining optimal ratio of reduced/oxidized glutathione level (GSH/GSSG) in erythrocytes, these results could indicate that in spite of numerous beneficial effects of fluoxetine, it may compromise both haemoglobin function and oxygen transport.",
journal = "Acta Chimica Slovenica",
title = "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats",
volume = "58",
number = "4",
pages = "785-791",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4640"
}

Adžić, M., Đorđević, J. D., Mitić, M., Simić, I., Rackov, G., Đorđević, A. D., Elaković, I., Matić, G.,& Radojčić, M.. (2011). Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica, 58(4), 785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640

Adžić M, Đorđević JD, Mitić M, Simić I, Rackov G, Đorđević AD, Elaković I, Matić G, Radojčić M. Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats. in Acta Chimica Slovenica. 2011;58(4):785-791.
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

Adžić, Miroslav, Đorđević, Jelena D., Mitić, Miloš, Simić, Iva, Rackov, Gorjana, Đorđević, Ana D., Elaković, Ivana, Matić, Gordana, Radojčić, Marija, "Fluoxetine Decreases Glutathione Reductase in Erythrocytes of Chronically Isolated Wistar Rats" in Acta Chimica Slovenica, 58, no. 4 (2011):785-791,
https://hdl.handle.net/21.15107/rcub_vinar_4640 .

TY  - CHAP
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
AU  - Nićiforović, Ana
AU  - Đorđević, Jelena
AU  - Đorđević, Ana
AU  - Demonacos, Constantinos
AU  - Krstić-Demonacos, Marija
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12040
AB  - Chronic stress is recognized as an etiological factor for the onset and exacerbation of
many psychiatric disorders. Among chronic stressors, those of psychosocial and
emotional origin are considered of particular importance for prominent depletion of
physiological and psychological resources. The key mechanisms underlying deleterious
effects of chronic stress are thought to emerge from the compromised stress response at
the level of hypothalamic-pituitary-adrenal (HPA) axis feedback, and limbic brain
structures, such as hippocampus (HIPPO) and prefrontal cortex (PFC).
In this review we summarize and discuss effects of chronic psychosocial isolation
(CPSI) using animal model of male Wistar rats, housed individually for 21 days lacking
physical and visual contact. CPSI, as an important distress factor for normally gregarious
Wistar rats, resulted in diminishment of serum corticosterone and blood glucose, and did
not alter catecholamine levels, which opposes most other chronic stressors that elevate
stress hormones. In the context of possibly aberrant feedback mechanism at the molecular
level, we discuss altered glucocorticoid receptor (GR) distribution and appearance of GR
phosphoisoform excessively phosphorylated on serine 232 (pGR S232), as well as,
altered activities of JNK and CDK kinases that target GR for phosphorylation. The
appearance of pGR S232 in the nucleus and the mitochondria of HIPPO and PFC is
potentially related to a marked transcriptional activation/repression of several GR
regulated nuclear genes (GR itself, CRH, BDNF) and mitochondrial genes (COX1,
COX3). Another important stress and redox state sensitive transcription factor, nuclear factor kappa B (NFțB) is also discussed in terms of the disturbed redox balance
(illustrated by the altered ratio of the activity of an array of antioxidant enzymes) and
altered proapoptotic/proplastic signalling, since it regulates transcription of a wide array
of genes (like Bcl-2, NCAM). Such cellular conditions, provoked by CPSI, are also
shown to affect susceptibility to mitochondrially triggered apoptosis (illustrated by
redistribution of Bcl family members and DNA fragmentation, more prominent in the
PFC) and to simultaneously affect expression of main neural plasticity protein,
polysialylated NCAM (PSA-NCAM). In summary, we present novel causal connection
between the redox imbalance in the CNS, altered signalling via JNK and CDK kinases,
GR phosphorylation/transactivity and NFțB transactivity, as well as their cellular
imbalance, the parameters which all together yield inadequate CNS and systemic stress
response.
T2  - Horizons in Neuroscience Research
T1  - Effects of Chronic Psychosocial Isolation on Limbic Brain Structures of Wistar Rats
VL  - 5
SP  - 97
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_vinar_12040
ER  - 

@inbook{
author = "Radojčić, Marija and Adžić, Miroslav and Nićiforović, Ana and Đorđević, Jelena and Đorđević, Ana and Demonacos, Constantinos and Krstić-Demonacos, Marija",
year = "2011",
abstract = "Chronic stress is recognized as an etiological factor for the onset and exacerbation of
many psychiatric disorders. Among chronic stressors, those of psychosocial and
emotional origin are considered of particular importance for prominent depletion of
physiological and psychological resources. The key mechanisms underlying deleterious
effects of chronic stress are thought to emerge from the compromised stress response at
the level of hypothalamic-pituitary-adrenal (HPA) axis feedback, and limbic brain
structures, such as hippocampus (HIPPO) and prefrontal cortex (PFC).
In this review we summarize and discuss effects of chronic psychosocial isolation
(CPSI) using animal model of male Wistar rats, housed individually for 21 days lacking
physical and visual contact. CPSI, as an important distress factor for normally gregarious
Wistar rats, resulted in diminishment of serum corticosterone and blood glucose, and did
not alter catecholamine levels, which opposes most other chronic stressors that elevate
stress hormones. In the context of possibly aberrant feedback mechanism at the molecular
level, we discuss altered glucocorticoid receptor (GR) distribution and appearance of GR
phosphoisoform excessively phosphorylated on serine 232 (pGR S232), as well as,
altered activities of JNK and CDK kinases that target GR for phosphorylation. The
appearance of pGR S232 in the nucleus and the mitochondria of HIPPO and PFC is
potentially related to a marked transcriptional activation/repression of several GR
regulated nuclear genes (GR itself, CRH, BDNF) and mitochondrial genes (COX1,
COX3). Another important stress and redox state sensitive transcription factor, nuclear factor kappa B (NFțB) is also discussed in terms of the disturbed redox balance
(illustrated by the altered ratio of the activity of an array of antioxidant enzymes) and
altered proapoptotic/proplastic signalling, since it regulates transcription of a wide array
of genes (like Bcl-2, NCAM). Such cellular conditions, provoked by CPSI, are also
shown to affect susceptibility to mitochondrially triggered apoptosis (illustrated by
redistribution of Bcl family members and DNA fragmentation, more prominent in the
PFC) and to simultaneously affect expression of main neural plasticity protein,
polysialylated NCAM (PSA-NCAM). In summary, we present novel causal connection
between the redox imbalance in the CNS, altered signalling via JNK and CDK kinases,
GR phosphorylation/transactivity and NFțB transactivity, as well as their cellular
imbalance, the parameters which all together yield inadequate CNS and systemic stress
response.",
journal = "Horizons in Neuroscience Research",
booktitle = "Effects of Chronic Psychosocial Isolation on Limbic Brain Structures of Wistar Rats",
volume = "5",
pages = "97-126",
url = "https://hdl.handle.net/21.15107/rcub_vinar_12040"
}

Radojčić, M., Adžić, M., Nićiforović, A., Đorđević, J., Đorđević, A., Demonacos, C.,& Krstić-Demonacos, M.. (2011). Effects of Chronic Psychosocial Isolation on Limbic Brain Structures of Wistar Rats. in Horizons in Neuroscience Research, 5, 97-126.
https://hdl.handle.net/21.15107/rcub_vinar_12040

Radojčić M, Adžić M, Nićiforović A, Đorđević J, Đorđević A, Demonacos C, Krstić-Demonacos M. Effects of Chronic Psychosocial Isolation on Limbic Brain Structures of Wistar Rats. in Horizons in Neuroscience Research. 2011;5:97-126.
https://hdl.handle.net/21.15107/rcub_vinar_12040 .

Radojčić, Marija, Adžić, Miroslav, Nićiforović, Ana, Đorđević, Jelena, Đorđević, Ana, Demonacos, Constantinos, Krstić-Demonacos, Marija, "Effects of Chronic Psychosocial Isolation on Limbic Brain Structures of Wistar Rats" in Horizons in Neuroscience Research, 5 (2011):97-126,
https://hdl.handle.net/21.15107/rcub_vinar_12040 .

TY  - JOUR
AU  - Elaković, Ivana
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
AU  - Matić, Gordana
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4277
AB  - Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.
T2  - Brain Research
T1  - Gender-specific response of brain corticosteroid receptors to stress and fluoxetine
VL  - 1384
SP  - 61
EP  - 68
DO  - 10.1016/j.brainres.2011.01.078
ER  - 

@article{
author = "Elaković, Ivana and Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija and Matić, Gordana",
year = "2011",
abstract = "Gender-related differences in dexamethasone binding to corticosteroid receptors (CR) and in glucocorticoid receptor (GR) protein level in the pituitary, hypothalamus, hippocampus and prefrontal cortex were studied before and after antidepressant fluoxetine administration to both unstressed and rats exposed to a chronic social isolation stress. Untreated males, in comparison to females, displayed higher hormone-binding capacity of both GR and mineralocorticoid receptor (MR) in the hippocampal cytosol, as well as higher GR protein level in the pituitary cytosol. In both genders, dexamethasone binding to MR exceeded that to GR. While fluoxetine treatment and social isolation had no effect on GR activity, the influence on MR was gender-specific. Fluoxetine facilitated MR hormone-binding only in females, increasing the MR/GA activity ratio. In contrast, after a 6-week isolation of males, MR binding capacity was diminished and MR/GR ratio inverted in favor of GR In addition, fluoxetine induced elevation of cytosolic GR protein level in the pituitary and hypothalamus, the latter change being gender-specific. The results point to gender-related differences in the CRs functioning and suggest that both MR and GR may contribute to well-known sexual dimorphism in vulnerability to stress and stress-related disorders and in the outcome of antidepressant treatment. (C) 2011 Elsevier B.V. All rights reserved.",
journal = "Brain Research",
title = "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine",
volume = "1384",
pages = "61-68",
doi = "10.1016/j.brainres.2011.01.078"
}

Elaković, I., Đorđević, A. D., Adžić, M., Đorđević, J. D., Radojčić, M.,& Matić, G.. (2011). Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research, 1384, 61-68.
https://doi.org/10.1016/j.brainres.2011.01.078

Elaković I, Đorđević AD, Adžić M, Đorđević JD, Radojčić M, Matić G. Gender-specific response of brain corticosteroid receptors to stress and fluoxetine. in Brain Research. 2011;1384:61-68.
doi:10.1016/j.brainres.2011.01.078 .

Elaković, Ivana, Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, Matić, Gordana, "Gender-specific response of brain corticosteroid receptors to stress and fluoxetine" in Brain Research, 1384 (2011):61-68,
https://doi.org/10.1016/j.brainres.2011.01.078 . .

TY  - JOUR
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Đorđević, Jelena D.
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4604
AB  - Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the pathophysiology of depression and stress disorders. Glucocorticoids, key regulators of the stress response, exert diverse effects on cellular processes in the hippocampus. Beside non-genomic pathways, glucocorticoid effects are mediated through activation of the glucocorticoid receptor (GR), a ligand activated transcriptional factor that belongs to the nuclear hormone receptor superfamily. We analysed the GR protein levels both in the cytoplasmic and nuclear compartments of the hippocampus of Wistar rats exposed to chronic psychosocial isolation stress upon chronic fluoxetine (FLU) treatment. Under chronic stress, corticosterone levels (CORT) were decreased compared to the control, and treatment with FLU did not change its level in the stressed rats. At the molecular level, FLU normalized the level of nuclear GR protein in the hippocampus of the stressed rats. Discrepancy between normalization of nuclear GR in the hippocampus and lack of normalization of HPA axis activity judged by CORT, suggests that other brain structures such as the amygdale and prefrontal cortex that also regulate HPA axis activity, seem not to be normalized by the FLU treatment used in our study.
T2  - Russian Journal of Physical Chemistry A
T1  - The antidepressant fluoxetine normalizes the nuclear glucocorticoid receptor evoked by psychosocial stress
VL  - 85
IS  - 13
SP  - 2422
EP  - 2425
DO  - 10.1134/S0036024411130152
ER  - 

@article{
author = "Mitić, Miloš and Simić, Iva and Đorđević, Jelena D. and Radojčić, Marija and Adžić, Miroslav",
year = "2011",
abstract = "Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the pathophysiology of depression and stress disorders. Glucocorticoids, key regulators of the stress response, exert diverse effects on cellular processes in the hippocampus. Beside non-genomic pathways, glucocorticoid effects are mediated through activation of the glucocorticoid receptor (GR), a ligand activated transcriptional factor that belongs to the nuclear hormone receptor superfamily. We analysed the GR protein levels both in the cytoplasmic and nuclear compartments of the hippocampus of Wistar rats exposed to chronic psychosocial isolation stress upon chronic fluoxetine (FLU) treatment. Under chronic stress, corticosterone levels (CORT) were decreased compared to the control, and treatment with FLU did not change its level in the stressed rats. At the molecular level, FLU normalized the level of nuclear GR protein in the hippocampus of the stressed rats. Discrepancy between normalization of nuclear GR in the hippocampus and lack of normalization of HPA axis activity judged by CORT, suggests that other brain structures such as the amygdale and prefrontal cortex that also regulate HPA axis activity, seem not to be normalized by the FLU treatment used in our study.",
journal = "Russian Journal of Physical Chemistry A",
title = "The antidepressant fluoxetine normalizes the nuclear glucocorticoid receptor evoked by psychosocial stress",
volume = "85",
number = "13",
pages = "2422-2425",
doi = "10.1134/S0036024411130152"
}

Mitić, M., Simić, I., Đorđević, J. D., Radojčić, M.,& Adžić, M.. (2011). The antidepressant fluoxetine normalizes the nuclear glucocorticoid receptor evoked by psychosocial stress. in Russian Journal of Physical Chemistry A, 85(13), 2422-2425.
https://doi.org/10.1134/S0036024411130152

Mitić M, Simić I, Đorđević JD, Radojčić M, Adžić M. The antidepressant fluoxetine normalizes the nuclear glucocorticoid receptor evoked by psychosocial stress. in Russian Journal of Physical Chemistry A. 2011;85(13):2422-2425.
doi:10.1134/S0036024411130152 .

Mitić, Miloš, Simić, Iva, Đorđević, Jelena D., Radojčić, Marija, Adžić, Miroslav, "The antidepressant fluoxetine normalizes the nuclear glucocorticoid receptor evoked by psychosocial stress" in Russian Journal of Physical Chemistry A, 85, no. 13 (2011):2422-2425,
https://doi.org/10.1134/S0036024411130152 . .

TY  - CONF
AU  - Adžić, Miroslav
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena
AU  - Elaković, Ivana
AU  - Simić, Iva
AU  - Mitić, Miloš
AU  - Rackov, Gorjana
AU  - Matić, Gordana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9306
AB  - Alterations in the antioxidative defense parameters upon chronic stress are considered
critical for pathophysiology of stress related psychiatric disorders and their status in
blood serves as biomarker for effects of pharmacological treatments. We investigated
the modulation of erythrocyte antioxidant enzymes (AOEs): superoxide dismutase
(SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR)
protein expression and activity in Wistar male rats subjected to chronic psychosocial
isolation and/or treated with fluoxetine. Chronically isolated animals exhibited
decreased levels of plasma corticoserone (CORT). AOEs status was not altered either
by chronic social isolation or by fluoxetine. The only exception was GLR, whose level
and activity were both markedly reduced by fluoxetine. Our study indicates that
fluoxetine treatment of chronically isolated male Wistar rats, leads to significant
reduction in the level and activity of GLR in the erythrocytes.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9306
ER  - 

@conference{
author = "Adžić, Miroslav and Đorđević, Ana D. and Đorđević, Jelena and Elaković, Ivana and Simić, Iva and Mitić, Miloš and Rackov, Gorjana and Matić, Gordana and Radojčić, Marija",
year = "2010",
abstract = "Alterations in the antioxidative defense parameters upon chronic stress are considered
critical for pathophysiology of stress related psychiatric disorders and their status in
blood serves as biomarker for effects of pharmacological treatments. We investigated
the modulation of erythrocyte antioxidant enzymes (AOEs): superoxide dismutase
(SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR)
protein expression and activity in Wistar male rats subjected to chronic psychosocial
isolation and/or treated with fluoxetine. Chronically isolated animals exhibited
decreased levels of plasma corticoserone (CORT). AOEs status was not altered either
by chronic social isolation or by fluoxetine. The only exception was GLR, whose level
and activity were both markedly reduced by fluoxetine. Our study indicates that
fluoxetine treatment of chronically isolated male Wistar rats, leads to significant
reduction in the level and activity of GLR in the erythrocytes.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9306"
}

Adžić, M., Đorđević, A. D., Đorđević, J., Elaković, I., Simić, I., Mitić, M., Rackov, G., Matić, G.,& Radojčić, M.. (2010). Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9306

Adžić M, Đorđević AD, Đorđević J, Elaković I, Simić I, Mitić M, Rackov G, Matić G, Radojčić M. Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9306 .

Adžić, Miroslav, Đorđević, Ana D., Đorđević, Jelena, Elaković, Ivana, Simić, Iva, Mitić, Miloš, Rackov, Gorjana, Matić, Gordana, Radojčić, Marija, "Fluoxetine decreases glutathione reductase in erythrocytes of chronically isolated wistar rats" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9306 .

TY  - CONF
AU  - Mitić, Miloš
AU  - Simić, Iva
AU  - Đorđević, Ana D.
AU  - Đorđević, J.
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9320
AB  - Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been
implicated in the pathophysiology of depression and stress disorders.
Glucocorticoids, key regulators of stress response, have diverse effects on cellular
processes in the hippocampus. Beside non genomic pathways, glucocorticoids
effects are mediated through activation of the glucocorticoid receptor (GR), a
ligand activated transcriptional factor that belongs to the nuclear hormone receptor
superfamily. We analysed the GR protein level both, in the cytoplasmic and
nuclear compartments in Wistar rat hippocampus, exposed to 3 week social
isolation stress upon chronic fluoxetine treatment. Under chronic stress,
corticosterone level was decreased compared to the control and treatment with
fluoxetine did not change its level significantly in stressed animals. At the
molecular level, fluoxetine significantly decreased the level of nuclear GR protein
in the brain hippocampus of the chronically stressed rats. Fluoxetine reversed the
nuclear level of GR disrupted by chronic psychosocial isolation (CPSI), but it
failed to normalize HPA axis activity.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9320
ER  - 

@conference{
author = "Mitić, Miloš and Simić, Iva and Đorđević, Ana D. and Đorđević, J. and Radojčić, Marija and Adžić, Miroslav",
year = "2010",
abstract = "Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has been
implicated in the pathophysiology of depression and stress disorders.
Glucocorticoids, key regulators of stress response, have diverse effects on cellular
processes in the hippocampus. Beside non genomic pathways, glucocorticoids
effects are mediated through activation of the glucocorticoid receptor (GR), a
ligand activated transcriptional factor that belongs to the nuclear hormone receptor
superfamily. We analysed the GR protein level both, in the cytoplasmic and
nuclear compartments in Wistar rat hippocampus, exposed to 3 week social
isolation stress upon chronic fluoxetine treatment. Under chronic stress,
corticosterone level was decreased compared to the control and treatment with
fluoxetine did not change its level significantly in stressed animals. At the
molecular level, fluoxetine significantly decreased the level of nuclear GR protein
in the brain hippocampus of the chronically stressed rats. Fluoxetine reversed the
nuclear level of GR disrupted by chronic psychosocial isolation (CPSI), but it
failed to normalize HPA axis activity.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9320"
}

Mitić, M., Simić, I., Đorđević, A. D., Đorđević, J., Radojčić, M.,& Adžić, M.. (2010). Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9320

Mitić M, Simić I, Đorđević AD, Đorđević J, Radojčić M, Adžić M. Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9320 .

Mitić, Miloš, Simić, Iva, Đorđević, Ana D., Đorđević, J., Radojčić, Marija, Adžić, Miroslav, "Fluoxetine decreases the level of nuclear glucocorticoid receptor in wistar rat hippocampus under chronic stress" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9320 .

TY  - CONF
AU  - Simić, Iva
AU  - Đorđević, Ana D.
AU  - Đorđević, Jelena
AU  - Mitić, Miloš
AU  - Radojčić, Marija
AU  - Adžić, Miroslav
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9323
AB  - It is known that chronic psychosocial isolation (CPSI) exerts maladaptive effect on the
hypothalamic-pituitary-adrenal (HPA) axis activity. Since the hypothalamus (HT) is a
major driver of the HPA axis activity and since glucocorticoid receptor protein (GR)
mediates HPA axis negative feedback particularly in this structure, we studied the
effect of CPSI by following the expression of GR and its chaperones hsp70 and hsp90
in HT. Our results showed that the ratios of HSPs/GR set by the CPSI were altered in
response to a novel acute stress, which indicated negative CPSI influence on GR
functions in HT.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
T1  - Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9323
ER  - 

@conference{
author = "Simić, Iva and Đorđević, Ana D. and Đorđević, Jelena and Mitić, Miloš and Radojčić, Marija and Adžić, Miroslav",
year = "2010",
abstract = "It is known that chronic psychosocial isolation (CPSI) exerts maladaptive effect on the
hypothalamic-pituitary-adrenal (HPA) axis activity. Since the hypothalamus (HT) is a
major driver of the HPA axis activity and since glucocorticoid receptor protein (GR)
mediates HPA axis negative feedback particularly in this structure, we studied the
effect of CPSI by following the expression of GR and its chaperones hsp70 and hsp90
in HT. Our results showed that the ratios of HSPs/GR set by the CPSI were altered in
response to a novel acute stress, which indicated negative CPSI influence on GR
functions in HT.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry",
title = "Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9323"
}

Simić, I., Đorđević, A. D., Đorđević, J., Mitić, M., Radojčić, M.,& Adžić, M.. (2010). Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia..
https://hdl.handle.net/21.15107/rcub_vinar_9323

Simić I, Đorđević AD, Đorđević J, Mitić M, Radojčić M, Adžić M. Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus. in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry. 2010;.
https://hdl.handle.net/21.15107/rcub_vinar_9323 .

Simić, Iva, Đorđević, Ana D., Đorđević, Jelena, Mitić, Miloš, Radojčić, Marija, Adžić, Miroslav, "Chronic psychosocial isolation alters hsp70/gr and hsp90/gr ratios in response to novel acute stress in rat hypothalamus" in Physical chemistry 2010 : 10th international conference on fundamental and applied aspects of physical chemistry (2010),
https://hdl.handle.net/21.15107/rcub_vinar_9323 .

TY  - JOUR
AU  - Đorđević, Jelena D.
AU  - Đorđević, Ana D.
AU  - Adžić, Miroslav
AU  - Nićiforović, Ana
AU  - Radojčić, Marija
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4153
AB  - Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.
T2  - Physiological Research
T1  - Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats
VL  - 59
IS  - 5
SP  - 729
EP  - 736
UR  - https://hdl.handle.net/21.15107/rcub_vinar_4153
ER  - 

@article{
author = "Đorđević, Jelena D. and Đorđević, Ana D. and Adžić, Miroslav and Nićiforović, Ana and Radojčić, Marija",
year = "2010",
abstract = "Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.",
journal = "Physiological Research",
title = "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats",
volume = "59",
number = "5",
pages = "729-736",
url = "https://hdl.handle.net/21.15107/rcub_vinar_4153"
}

Đorđević, J. D., Đorđević, A. D., Adžić, M., Nićiforović, A.,& Radojčić, M.. (2010). Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats. in Physiological Research, 59(5), 729-736.
https://hdl.handle.net/21.15107/rcub_vinar_4153

Đorđević JD, Đorđević AD, Adžić M, Nićiforović A, Radojčić M. Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats. in Physiological Research. 2010;59(5):729-736.
https://hdl.handle.net/21.15107/rcub_vinar_4153 .

Đorđević, Jelena D., Đorđević, Ana D., Adžić, Miroslav, Nićiforović, Ana, Radojčić, Marija, "Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats" in Physiological Research, 59, no. 5 (2010):729-736,
https://hdl.handle.net/21.15107/rcub_vinar_4153 .