TY  - JOUR
AU  - Stanisavljević, Andrijana
AU  - Perić, Ivana
AU  - Bernardi, Rick E.
AU  - Gass, Peter
AU  - Filipović, Dragana
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8386
AB  - Chronic social stress and/or pharmacological treatments differentially modulate the expression of c-Fos, a marker of neuronal activity, in subregions of the rat brain. Here, we examined the effect of the atypical antipsychotic Clozapine (Clz) (20 mg/kg/day for 3 weeks) on the neuronal activation pattern of c-Fos protein expression in stress-relevant brain subregions of adult male Wistar rats exposed to chronic social isolation (CSIS: 3 weeks), an animal model of depression and schizophrenia, and controls. The protein expression of c-Fos was also used to map neuronal populations in brain subregions activated by CSIS alone. Subregions which showed significantly increased c-Fos protein expression following CSIS included the retrosplenial cortex (RSC), (subregions:RSC granular cortex, c region (RSGc) and dysgranular (RSD)), dentate gyrus, dorsal (DGd), paraventricular thalamic nucleus, posterior part (PVP), lateral (LA)/basolateral (BL) complex of amygdala, caudate putamen (CPu) and accumbens nucleus, shell (AcbSh). Increases in c-Fos protein expression in the RSGc, RSD, DGd, PVP, LA/BL complex of amygdala and striatum (CPu, Acb Core (AcbC) and AcbSh) following Clz treatment in controls were found. Clz applied simultaneously with CSIS modulated neuronal activity in CPu, AcbC and AcbSh subregions compared to CSIS alone, increasing c-Fos protein expression. Furthermore, Clz revealed synergistic effects with CSIS in the CA1d and PVP. These identified neural circuits reflect brain subregions activated following CSIS and/or Clz administration. These data further contribute to the understanding of the effectiveness of Clz in the modulation of brain subregion activation in response to CSIS. © 2019
T2  - Brain Research Bulletin
T1  - Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats
VL  - 152
SP  - 35
EP  - 44
DO  - 10.1016/j.brainresbull.2019.07.005
ER  - 

@article{
author = "Stanisavljević, Andrijana and Perić, Ivana and Bernardi, Rick E. and Gass, Peter and Filipović, Dragana",
year = "2019",
abstract = "Chronic social stress and/or pharmacological treatments differentially modulate the expression of c-Fos, a marker of neuronal activity, in subregions of the rat brain. Here, we examined the effect of the atypical antipsychotic Clozapine (Clz) (20 mg/kg/day for 3 weeks) on the neuronal activation pattern of c-Fos protein expression in stress-relevant brain subregions of adult male Wistar rats exposed to chronic social isolation (CSIS: 3 weeks), an animal model of depression and schizophrenia, and controls. The protein expression of c-Fos was also used to map neuronal populations in brain subregions activated by CSIS alone. Subregions which showed significantly increased c-Fos protein expression following CSIS included the retrosplenial cortex (RSC), (subregions:RSC granular cortex, c region (RSGc) and dysgranular (RSD)), dentate gyrus, dorsal (DGd), paraventricular thalamic nucleus, posterior part (PVP), lateral (LA)/basolateral (BL) complex of amygdala, caudate putamen (CPu) and accumbens nucleus, shell (AcbSh). Increases in c-Fos protein expression in the RSGc, RSD, DGd, PVP, LA/BL complex of amygdala and striatum (CPu, Acb Core (AcbC) and AcbSh) following Clz treatment in controls were found. Clz applied simultaneously with CSIS modulated neuronal activity in CPu, AcbC and AcbSh subregions compared to CSIS alone, increasing c-Fos protein expression. Furthermore, Clz revealed synergistic effects with CSIS in the CA1d and PVP. These identified neural circuits reflect brain subregions activated following CSIS and/or Clz administration. These data further contribute to the understanding of the effectiveness of Clz in the modulation of brain subregion activation in response to CSIS. © 2019",
journal = "Brain Research Bulletin",
title = "Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats",
volume = "152",
pages = "35-44",
doi = "10.1016/j.brainresbull.2019.07.005"
}

Stanisavljević, A., Perić, I., Bernardi, R. E., Gass, P.,& Filipović, D.. (2019). Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats. in Brain Research Bulletin, 152, 35-44.
https://doi.org/10.1016/j.brainresbull.2019.07.005

Stanisavljević A, Perić I, Bernardi RE, Gass P, Filipović D. Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats. in Brain Research Bulletin. 2019;152:35-44.
doi:10.1016/j.brainresbull.2019.07.005 .

Stanisavljević, Andrijana, Perić, Ivana, Bernardi, Rick E., Gass, Peter, Filipović, Dragana, "Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats" in Brain Research Bulletin, 152 (2019):35-44,
https://doi.org/10.1016/j.brainresbull.2019.07.005 . .

TY  - JOUR
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7584
AB  - The dysfunction of parvalbumin-positive (PV+) interneurons, the most abundant type of hippocampal GABAergic inhibitory interneuron, has been implicated in mood disorders. We recently reported that adult male Wistar rats exposed to three weeks of social isolation show depressive-and anxiety-like behaviors and a reduced number of PV+ interneurons in all hippocampal subregions. As GABA neurotransmission has been proposed as a potential therapeutic target of antidepressant and antipsychotic medications, we examined whether treatment with the antidepressant fluoxetine (Flx) (15 mg/kg/day) or the antipsychotic clozapine (Clz) (20 mg/kg/day) during three weeks of social isolation in rats offered protection from the isolation stress-induced reduction in the number of PV+ interneurons in hippocampal subregions. Using immunofluorescence analysis, we revealed that both chronic Flx and Clz partially prevented the isolation-induced changes. Flx prevented the reduction in the number of PV+ interneurons in the CA2, CA3, without affecting the CA1 and dentate gyrus DG areas, whereas Clz prevented this decrement in the CA2, CA3 and DG regions but not in CA1 areas. Moreover, Flx increased the number of PV+ interneurons in CA1 in control animals. These findings suggest that chronic administration of Flx or Clz may offer partial protection from social isolation stress via modulation of the hippocampal GABAergic system. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
T2  - Neuroscience
T1  - Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus
VL  - 371
SP  - 384
EP  - 394
DO  - 10.1016/j.neuroscience.2017.12.020
ER  - 

@article{
year = "2018",
abstract = "The dysfunction of parvalbumin-positive (PV+) interneurons, the most abundant type of hippocampal GABAergic inhibitory interneuron, has been implicated in mood disorders. We recently reported that adult male Wistar rats exposed to three weeks of social isolation show depressive-and anxiety-like behaviors and a reduced number of PV+ interneurons in all hippocampal subregions. As GABA neurotransmission has been proposed as a potential therapeutic target of antidepressant and antipsychotic medications, we examined whether treatment with the antidepressant fluoxetine (Flx) (15 mg/kg/day) or the antipsychotic clozapine (Clz) (20 mg/kg/day) during three weeks of social isolation in rats offered protection from the isolation stress-induced reduction in the number of PV+ interneurons in hippocampal subregions. Using immunofluorescence analysis, we revealed that both chronic Flx and Clz partially prevented the isolation-induced changes. Flx prevented the reduction in the number of PV+ interneurons in the CA2, CA3, without affecting the CA1 and dentate gyrus DG areas, whereas Clz prevented this decrement in the CA2, CA3 and DG regions but not in CA1 areas. Moreover, Flx increased the number of PV+ interneurons in CA1 in control animals. These findings suggest that chronic administration of Flx or Clz may offer partial protection from social isolation stress via modulation of the hippocampal GABAergic system. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.",
journal = "Neuroscience",
title = "Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus",
volume = "371",
pages = "384-394",
doi = "10.1016/j.neuroscience.2017.12.020"
}

(2018). Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus. in Neuroscience, 371, 384-394.
https://doi.org/10.1016/j.neuroscience.2017.12.020

Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus. in Neuroscience. 2018;371:384-394.
doi:10.1016/j.neuroscience.2017.12.020 .

"Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus" in Neuroscience, 371 (2018):384-394,
https://doi.org/10.1016/j.neuroscience.2017.12.020 . .

TY  - JOUR
AU  - Filipović, Dragana
AU  - Todorović, Nevena
AU  - Bernardi, Rick E.
AU  - Gass, Peter
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1392
AB  - Various stressors may disrupt the redox homeostasis of an organism by causing oxidative and nitrosative stress that may activate stressor-specific pathways and provoke specific responses. Chronic social isolation (CSIS) represents a mild chronic stress that evokes a variety of neurobehavioral changes in rats similar to those observed in people with psychiatric disorders, including depression. Most rodent studies have focused on the effect of social isolation during weaning or adolescence, while its effect in adult rats has not been extensively examined. In this review, we discuss the current knowledge regarding the involvement of oxidative/nitrosative stress pathways in the prefrontal cortex and hippocampus of adult male rats exposed to CSIS, focusing on hypothalamic-pituitary-adrenocortical (HPA) axis activity, behavior parameters, antioxidative defense systems, stress signaling mediated by nuclear factor-kappa B (NF-kappa B), and mitochondria-related proapoptotic signaling. Although increased concentrations of corticosterone (CORT) have been shown to induce oxidative and nitrosative stress, we suggest a mechanism underlying the glucocorticoid paradox whereby a state of oxidative/nitrosative stress may exist under basal CORT levels. This review also highlights the differential susceptibility of prefrontal cortex and hippocampus to oxidative stress following CSIS and suggests a possible cellular pathway of stress tolerance that preserves the hippocampus from molecular damage and apoptosis. The differential regulation of the transcriptional factor NF-kappa B, and the enzymes inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) following CSIS may be one functional difference between the response of the prefrontal cortex and hippocampus, thus identifying potentially relevant targets for antidepressant treatment.
T2  - Brain Structure and Function
T1  - Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms
VL  - 222
IS  - 1
SP  - 1
EP  - 20
DO  - 10.1007/s00429-016-1218-9
ER  - 

@article{
author = "Filipović, Dragana and Todorović, Nevena and Bernardi, Rick E. and Gass, Peter",
year = "2017",
abstract = "Various stressors may disrupt the redox homeostasis of an organism by causing oxidative and nitrosative stress that may activate stressor-specific pathways and provoke specific responses. Chronic social isolation (CSIS) represents a mild chronic stress that evokes a variety of neurobehavioral changes in rats similar to those observed in people with psychiatric disorders, including depression. Most rodent studies have focused on the effect of social isolation during weaning or adolescence, while its effect in adult rats has not been extensively examined. In this review, we discuss the current knowledge regarding the involvement of oxidative/nitrosative stress pathways in the prefrontal cortex and hippocampus of adult male rats exposed to CSIS, focusing on hypothalamic-pituitary-adrenocortical (HPA) axis activity, behavior parameters, antioxidative defense systems, stress signaling mediated by nuclear factor-kappa B (NF-kappa B), and mitochondria-related proapoptotic signaling. Although increased concentrations of corticosterone (CORT) have been shown to induce oxidative and nitrosative stress, we suggest a mechanism underlying the glucocorticoid paradox whereby a state of oxidative/nitrosative stress may exist under basal CORT levels. This review also highlights the differential susceptibility of prefrontal cortex and hippocampus to oxidative stress following CSIS and suggests a possible cellular pathway of stress tolerance that preserves the hippocampus from molecular damage and apoptosis. The differential regulation of the transcriptional factor NF-kappa B, and the enzymes inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) following CSIS may be one functional difference between the response of the prefrontal cortex and hippocampus, thus identifying potentially relevant targets for antidepressant treatment.",
journal = "Brain Structure and Function",
title = "Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms",
volume = "222",
number = "1",
pages = "1-20",
doi = "10.1007/s00429-016-1218-9"
}

Filipović, D., Todorović, N., Bernardi, R. E.,& Gass, P.. (2017). Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms. in Brain Structure and Function, 222(1), 1-20.
https://doi.org/10.1007/s00429-016-1218-9

Filipović D, Todorović N, Bernardi RE, Gass P. Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms. in Brain Structure and Function. 2017;222(1):1-20.
doi:10.1007/s00429-016-1218-9 .

Filipović, Dragana, Todorović, Nevena, Bernardi, Rick E., Gass, Peter, "Oxidative and nitrosative stress pathways in the brain of socially isolated adult male rats demonstrating depressive- and anxiety-like symptoms" in Brain Structure and Function, 222, no. 1 (2017):1-20,
https://doi.org/10.1007/s00429-016-1218-9 . .

TY  - JOUR
AU  - Martinović, Jelena
AU  - Bernardi, Rick E.
AU  - Filipović, Dragana
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5826
AB  - Stress-related glucocorticoids and glutamate release has been implicated in depression. Glutamate neurotoxicity is mediated, in part, by the production of nitric oxide via nitric oxide synthase (NOS) isoforms and mitochondrial damage. We previously reported that chronic social isolation stress triggers proapoptotic signaling in the rat prefrontal cortex, but not in the hippocampus. Given that the hippocampus is highly sensitive to stress, we examined signaling cascades underlying the hippocampal cellular protection through the NOS pathway, antioxidant capacity and heat shock protein (Hsp) expression. We investigated neuronal (nNOS) and inducible (iNOS) protein levels, subcellular protein distributions of nuclear factor-kappa B (NF-kappa B), CuZnSOD and MnSOD activity, reduced glutathione (GSH), stress-inducible Hsp70 (Hsp70i) protein expression and serum corticosterone (CORT) levels of rats exposed to 21 days of chronic social isolation, an animal model of depression, alone or in combination with 2 h of acute immobilization or cold stress (combined stress). Both acute stressors elevated CORT, with lesser magnitude increase in chronically isolated rats exposed to novel acute stress as compared to acute stressors alone, indicating compromised HPA axis activity. Acute cold decreased nuclear CuZnSOD activity and stimulated NF-kappa B nuclear translocation. Chronic social isolation resulted in no activation of NF-kappa B, but led to decreased GSH, iNOS and increased nNOS and Hsp70i levels, alterations that remained following combined stressors. Decreased mitochondrial MnSOD activity after combined stressors suggests compromised detoxifying capacity. These data indicate that Hsp70i upregulation may provide hippocampal cellular protection against chronic social isolation stress mediated by downregulation of iNOS protein expression through suppression of NF-kappa B activation.
T2  - Journal of Neural Transmission
T1  - Protective effect of Hsp70i against chronic social isolation stress in the rat hippocampus
VL  - 121
IS  - 1
SP  - 3
EP  - 14
DO  - 10.1007/s00702-013-1066-1
ER  - 

@article{
author = "Martinović, Jelena and Bernardi, Rick E. and Filipović, Dragana",
year = "2014",
abstract = "Stress-related glucocorticoids and glutamate release has been implicated in depression. Glutamate neurotoxicity is mediated, in part, by the production of nitric oxide via nitric oxide synthase (NOS) isoforms and mitochondrial damage. We previously reported that chronic social isolation stress triggers proapoptotic signaling in the rat prefrontal cortex, but not in the hippocampus. Given that the hippocampus is highly sensitive to stress, we examined signaling cascades underlying the hippocampal cellular protection through the NOS pathway, antioxidant capacity and heat shock protein (Hsp) expression. We investigated neuronal (nNOS) and inducible (iNOS) protein levels, subcellular protein distributions of nuclear factor-kappa B (NF-kappa B), CuZnSOD and MnSOD activity, reduced glutathione (GSH), stress-inducible Hsp70 (Hsp70i) protein expression and serum corticosterone (CORT) levels of rats exposed to 21 days of chronic social isolation, an animal model of depression, alone or in combination with 2 h of acute immobilization or cold stress (combined stress). Both acute stressors elevated CORT, with lesser magnitude increase in chronically isolated rats exposed to novel acute stress as compared to acute stressors alone, indicating compromised HPA axis activity. Acute cold decreased nuclear CuZnSOD activity and stimulated NF-kappa B nuclear translocation. Chronic social isolation resulted in no activation of NF-kappa B, but led to decreased GSH, iNOS and increased nNOS and Hsp70i levels, alterations that remained following combined stressors. Decreased mitochondrial MnSOD activity after combined stressors suggests compromised detoxifying capacity. These data indicate that Hsp70i upregulation may provide hippocampal cellular protection against chronic social isolation stress mediated by downregulation of iNOS protein expression through suppression of NF-kappa B activation.",
journal = "Journal of Neural Transmission",
title = "Protective effect of Hsp70i against chronic social isolation stress in the rat hippocampus",
volume = "121",
number = "1",
pages = "3-14",
doi = "10.1007/s00702-013-1066-1"
}

Martinović, J., Bernardi, R. E.,& Filipović, D.. (2014). Protective effect of Hsp70i against chronic social isolation stress in the rat hippocampus. in Journal of Neural Transmission, 121(1), 3-14.
https://doi.org/10.1007/s00702-013-1066-1

Martinović J, Bernardi RE, Filipović D. Protective effect of Hsp70i against chronic social isolation stress in the rat hippocampus. in Journal of Neural Transmission. 2014;121(1):3-14.
doi:10.1007/s00702-013-1066-1 .

Martinović, Jelena, Bernardi, Rick E., Filipović, Dragana, "Protective effect of Hsp70i against chronic social isolation stress in the rat hippocampus" in Journal of Neural Transmission, 121, no. 1 (2014):3-14,
https://doi.org/10.1007/s00702-013-1066-1 . .

TY  - JOUR
AU  - Martinović, Jelena
AU  - Todorović, Nevena
AU  - Tomanović, Nada
AU  - Bošković, Maja
AU  - Djordjevic, Snezana
AU  - Lazarević-Pašti, Tamara
AU  - Bernardi, Rick E.
AU  - Đurđević, Aleksandra
AU  - Filipović, Dragana
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6043
AB  - Chronic exposure to stress contributes to the etiology of mood disorders, and the liver as a target organ of antidepressant and antipsychotic drug metabolism is vulnerable to drug-induced toxicity. We investigated the effects of chronic administration of fluoxetine (15 mg/kg/day) or clozapine (20 mg/kg/day) on liver injury via the measurement of liver enzymes, oxidative stress and histopathology in rats exposed to chronic social isolation (21 days), an animal model of depression, and controls. The activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), the liver content of carbonyl groups, malonyldialdehyde (MDA), reduced glutathione (GSH), cytosolic glutathione S-transferase (GST) and nitric oxide (NO) metabolites were determined. We also characterized nuclear factor-kappa B (NF-kappa B), cyclooxygenase-2 (COX-2) and CuZn-superoxide dismutase (CuZnSOD) protein expression as well as histopathological changes. Increased serum ALT activity in chronically-isolated and control animals treated with both drugs was found while increased AST activity was observed only in fluoxetine-treated rats (chronically-isolated and controls). Increased carbonyl content, MDA, GST activity and decreased GSH levels in drug-treated controls/chronically-isolated animals suggest a link between drugs and hepatic oxidative stress. Increased NO levels associated with NF-kappa B activation and the concomitant increased COX-2 expression together with compromised CuZnSOD expression in clozapine-treated chronically-isolated rats likely reinforce oxidative stress, observed by increased lipid peroxidation and GSH depletion. In contrast, fluoxetine reduced NO levels in chronically-isolated rats. Isolation induced oxidative stress but histological changes were similar to those observed in vehicle-treated controls. Chronic administration of fluoxetine in both chronically-isolated and control animals resulted in more or less normal hepatic architecture, while clozapine in both groups resulted in liver injury. These data suggest that clozapine appears to have a higher potential to induce liver toxicity than fluoxetine. (C) 2014 Elsevier B.V. All rights reserved.
T2  - European Journal of Pharmaceutical Sciences
T1  - Chronic administration of fluoxetine or clozapine induces oxidative stress in rat liver: A histopathological study
VL  - 59
SP  - 20
EP  - 30
DO  - 10.1016/j.ejps.2014.04.010
ER  - 

@article{
author = "Martinović, Jelena and Todorović, Nevena and Tomanović, Nada and Bošković, Maja and Djordjevic, Snezana and Lazarević-Pašti, Tamara and Bernardi, Rick E. and Đurđević, Aleksandra and Filipović, Dragana",
year = "2014",
abstract = "Chronic exposure to stress contributes to the etiology of mood disorders, and the liver as a target organ of antidepressant and antipsychotic drug metabolism is vulnerable to drug-induced toxicity. We investigated the effects of chronic administration of fluoxetine (15 mg/kg/day) or clozapine (20 mg/kg/day) on liver injury via the measurement of liver enzymes, oxidative stress and histopathology in rats exposed to chronic social isolation (21 days), an animal model of depression, and controls. The activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), the liver content of carbonyl groups, malonyldialdehyde (MDA), reduced glutathione (GSH), cytosolic glutathione S-transferase (GST) and nitric oxide (NO) metabolites were determined. We also characterized nuclear factor-kappa B (NF-kappa B), cyclooxygenase-2 (COX-2) and CuZn-superoxide dismutase (CuZnSOD) protein expression as well as histopathological changes. Increased serum ALT activity in chronically-isolated and control animals treated with both drugs was found while increased AST activity was observed only in fluoxetine-treated rats (chronically-isolated and controls). Increased carbonyl content, MDA, GST activity and decreased GSH levels in drug-treated controls/chronically-isolated animals suggest a link between drugs and hepatic oxidative stress. Increased NO levels associated with NF-kappa B activation and the concomitant increased COX-2 expression together with compromised CuZnSOD expression in clozapine-treated chronically-isolated rats likely reinforce oxidative stress, observed by increased lipid peroxidation and GSH depletion. In contrast, fluoxetine reduced NO levels in chronically-isolated rats. Isolation induced oxidative stress but histological changes were similar to those observed in vehicle-treated controls. Chronic administration of fluoxetine in both chronically-isolated and control animals resulted in more or less normal hepatic architecture, while clozapine in both groups resulted in liver injury. These data suggest that clozapine appears to have a higher potential to induce liver toxicity than fluoxetine. (C) 2014 Elsevier B.V. All rights reserved.",
journal = "European Journal of Pharmaceutical Sciences",
title = "Chronic administration of fluoxetine or clozapine induces oxidative stress in rat liver: A histopathological study",
volume = "59",
pages = "20-30",
doi = "10.1016/j.ejps.2014.04.010"
}

Martinović, J., Todorović, N., Tomanović, N., Bošković, M., Djordjevic, S., Lazarević-Pašti, T., Bernardi, R. E., Đurđević, A.,& Filipović, D.. (2014). Chronic administration of fluoxetine or clozapine induces oxidative stress in rat liver: A histopathological study. in European Journal of Pharmaceutical Sciences, 59, 20-30.
https://doi.org/10.1016/j.ejps.2014.04.010

Martinović J, Todorović N, Tomanović N, Bošković M, Djordjevic S, Lazarević-Pašti T, Bernardi RE, Đurđević A, Filipović D. Chronic administration of fluoxetine or clozapine induces oxidative stress in rat liver: A histopathological study. in European Journal of Pharmaceutical Sciences. 2014;59:20-30.
doi:10.1016/j.ejps.2014.04.010 .

Martinović, Jelena, Todorović, Nevena, Tomanović, Nada, Bošković, Maja, Djordjevic, Snezana, Lazarević-Pašti, Tamara, Bernardi, Rick E., Đurđević, Aleksandra, Filipović, Dragana, "Chronic administration of fluoxetine or clozapine induces oxidative stress in rat liver: A histopathological study" in European Journal of Pharmaceutical Sciences, 59 (2014):20-30,
https://doi.org/10.1016/j.ejps.2014.04.010 . .