TY  - JOUR
AU  - Drakulić, Dunja R.
AU  - Velickovic, N.
AU  - Stanojlović, Miloš R.
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Lavrnja, I.
AU  - Horvat, Anica
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5549
AB  - Synthetic glucocorticoid dexamethasone (DEX), a highly potent anti-inflammatory and immunosuppressive agent, is widely used in the treatment of brain cancer, as well as for inflammatory and autoimmune diseases. The present study aimed to determine whether low-dose subchronic DEX treatment (100g/kg for eight consecutive days) exerts long-term effects on apoptosis in the adult rat prefrontal cortex (PFC) by examining the expression of cell death-promoting molecules [poly(ADP-ribose) polymerase (PARP), p53, procaspase 3, cleaved caspase 3, Bax] and cell-survival molecules (AKT, Bcl-2). The results obtained revealed that body, thymus and adrenal gland weights, as well corticosterone levels, in the serum and PFC were reduced 1day after the last DEX injection. In the PFC, DEX caused activation of AKT, augmentation of pro-survival Bcl-2 protein and an enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to the mitochondria. An unaltered profile with respect to the protein expression of apoptotic molecules PARP, procaspase 3 and Bax was detected, whereas p53 protein was decreased. Reverse transcriptase -polymerase chain reaction analysis showed a decrease of p53 mRNA levels and no significant difference in Bcl-2 and Bax mRNA expression in DEX-treated rats. Finally, a DNA fragmentation assay and Fluoro-Jade staining demonstrated no considerable changes in apoptosis in the rat PFC. Our findings support the concept that low-dose DEX creates a hypocorticoid state in the brain and also indicate that subchronic DEX treatment activates the pro-survival signalling pathway but does not change apoptotic markers in the rat PFC. This mechanism might be relevant for the DEX-induced apoptosis resistance observed during and after chemotherapy of patients with brain tumours.
T2  - Journal of Neuroendocrinology
T1  - Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex
VL  - 25
IS  - 7
SP  - 605
EP  - 616
DO  - 10.1111/jne.12037
ER  - 

@article{
author = "Drakulić, Dunja R. and Velickovic, N. and Stanojlović, Miloš R. and Grković, Ivana and Mitrović, Nataša Lj. and Lavrnja, I. and Horvat, Anica",
year = "2013",
abstract = "Synthetic glucocorticoid dexamethasone (DEX), a highly potent anti-inflammatory and immunosuppressive agent, is widely used in the treatment of brain cancer, as well as for inflammatory and autoimmune diseases. The present study aimed to determine whether low-dose subchronic DEX treatment (100g/kg for eight consecutive days) exerts long-term effects on apoptosis in the adult rat prefrontal cortex (PFC) by examining the expression of cell death-promoting molecules [poly(ADP-ribose) polymerase (PARP), p53, procaspase 3, cleaved caspase 3, Bax] and cell-survival molecules (AKT, Bcl-2). The results obtained revealed that body, thymus and adrenal gland weights, as well corticosterone levels, in the serum and PFC were reduced 1day after the last DEX injection. In the PFC, DEX caused activation of AKT, augmentation of pro-survival Bcl-2 protein and an enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to the mitochondria. An unaltered profile with respect to the protein expression of apoptotic molecules PARP, procaspase 3 and Bax was detected, whereas p53 protein was decreased. Reverse transcriptase -polymerase chain reaction analysis showed a decrease of p53 mRNA levels and no significant difference in Bcl-2 and Bax mRNA expression in DEX-treated rats. Finally, a DNA fragmentation assay and Fluoro-Jade staining demonstrated no considerable changes in apoptosis in the rat PFC. Our findings support the concept that low-dose DEX creates a hypocorticoid state in the brain and also indicate that subchronic DEX treatment activates the pro-survival signalling pathway but does not change apoptotic markers in the rat PFC. This mechanism might be relevant for the DEX-induced apoptosis resistance observed during and after chemotherapy of patients with brain tumours.",
journal = "Journal of Neuroendocrinology",
title = "Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex",
volume = "25",
number = "7",
pages = "605-616",
doi = "10.1111/jne.12037"
}

Drakulić, D. R., Velickovic, N., Stanojlović, M. R., Grković, I., Mitrović, N. Lj., Lavrnja, I.,& Horvat, A.. (2013). Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex. in Journal of Neuroendocrinology, 25(7), 605-616.
https://doi.org/10.1111/jne.12037

Drakulić DR, Velickovic N, Stanojlović MR, Grković I, Mitrović NL, Lavrnja I, Horvat A. Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex. in Journal of Neuroendocrinology. 2013;25(7):605-616.
doi:10.1111/jne.12037 .

Drakulić, Dunja R., Velickovic, N., Stanojlović, Miloš R., Grković, Ivana, Mitrović, Nataša Lj., Lavrnja, I., Horvat, Anica, "Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex" in Journal of Neuroendocrinology, 25, no. 7 (2013):605-616,
https://doi.org/10.1111/jne.12037 . .

TY  - JOUR
AU  - Petrović, S.
AU  - Velickovic, N.
AU  - Stanojević, Ivana
AU  - Milošević, Maja
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4512
AB  - Our results, as well as those of others, have indicated that 17 beta-estradiol (E2) exerts its nongenomic effects in neuronal cells by affecting plasma membrane Ca2+ flux. In neuronal cells mitochondria possess Ca2+ buffering properties as they both sequester and release Ca2+. The goal of this study was to examine the rapid non-genomic effect of E2 on mitochondria! Ca2+ transport in hippocampal synaptosomes from ovariectomised rats. In addition, we aimed to determine if, and to what extent, E2 receptors participated in mitochondria! Ca2+ transport modulation by E2 in vitro. E2-specific binding and Ca2+ transport was monitored. At physiological E2 concentrations (0.1-1.5 nmol/L), specific E2 binding to mitochondria isolated from hippocampal synaptosomes was detected with a B-max and K-m of 37.6 +/- 2.6 fmol/mg protein and 0.69 +/- 0.14 nmol/L of free E2, respectively. The main mitochondrial Ca2+ influx mechanism is the Ruthenium Red-sensitive uniporter driven by mitochondrial membrane potential. Despite no effect of E2 on Ca2+ influx, a physiological E2 concentration (0.5 nmol/L) protected mitochondrial membrane potential and consequently Ca2+ influx from the uncoupling agent carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (1 mu mol/L). In neuronal cells the predominant mitochondria! Ca2+ efflux mechanism is the Na+/Ca2+ exchanger. E2 caused Ca2+ efflux inhibition (by 46%) coupled with increased affinity of the Na+/Ca2+ exchanger for Na+. Using E2 receptor (ER alpha and ER beta) antagonists and agonists, we confirmed ER betas involvement in E2-induced mitochondrial membrane potential protection as well as Ca2+ efflux inhibition. In summary, our results indicate that the nongenomic neuromodulatory role of E2 in rat hippocampus is achieved by affecting mitochondria! Ca2+ transport via, in part, mitochondrial ER beta. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
T2  - Neuroscience
T1  - Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus
VL  - 192
SP  - 195
EP  - 204
DO  - 10.1016/j.neuroscience.2011.06.030
ER  - 

@article{
author = "Petrović, S. and Velickovic, N. and Stanojević, Ivana and Milošević, Maja and Drakulić, Dunja R. and Stanojlović, Miloš R. and Horvat, Anica",
year = "2011",
abstract = "Our results, as well as those of others, have indicated that 17 beta-estradiol (E2) exerts its nongenomic effects in neuronal cells by affecting plasma membrane Ca2+ flux. In neuronal cells mitochondria possess Ca2+ buffering properties as they both sequester and release Ca2+. The goal of this study was to examine the rapid non-genomic effect of E2 on mitochondria! Ca2+ transport in hippocampal synaptosomes from ovariectomised rats. In addition, we aimed to determine if, and to what extent, E2 receptors participated in mitochondria! Ca2+ transport modulation by E2 in vitro. E2-specific binding and Ca2+ transport was monitored. At physiological E2 concentrations (0.1-1.5 nmol/L), specific E2 binding to mitochondria isolated from hippocampal synaptosomes was detected with a B-max and K-m of 37.6 +/- 2.6 fmol/mg protein and 0.69 +/- 0.14 nmol/L of free E2, respectively. The main mitochondrial Ca2+ influx mechanism is the Ruthenium Red-sensitive uniporter driven by mitochondrial membrane potential. Despite no effect of E2 on Ca2+ influx, a physiological E2 concentration (0.5 nmol/L) protected mitochondrial membrane potential and consequently Ca2+ influx from the uncoupling agent carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (1 mu mol/L). In neuronal cells the predominant mitochondria! Ca2+ efflux mechanism is the Na+/Ca2+ exchanger. E2 caused Ca2+ efflux inhibition (by 46%) coupled with increased affinity of the Na+/Ca2+ exchanger for Na+. Using E2 receptor (ER alpha and ER beta) antagonists and agonists, we confirmed ER betas involvement in E2-induced mitochondrial membrane potential protection as well as Ca2+ efflux inhibition. In summary, our results indicate that the nongenomic neuromodulatory role of E2 in rat hippocampus is achieved by affecting mitochondria! Ca2+ transport via, in part, mitochondrial ER beta. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.",
journal = "Neuroscience",
title = "Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus",
volume = "192",
pages = "195-204",
doi = "10.1016/j.neuroscience.2011.06.030"
}

Petrović, S., Velickovic, N., Stanojević, I., Milošević, M., Drakulić, D. R., Stanojlović, M. R.,& Horvat, A.. (2011). Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus. in Neuroscience, 192, 195-204.
https://doi.org/10.1016/j.neuroscience.2011.06.030

Petrović S, Velickovic N, Stanojević I, Milošević M, Drakulić DR, Stanojlović MR, Horvat A. Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus. in Neuroscience. 2011;192:195-204.
doi:10.1016/j.neuroscience.2011.06.030 .

Petrović, S., Velickovic, N., Stanojević, Ivana, Milošević, Maja, Drakulić, Dunja R., Stanojlović, Miloš R., Horvat, Anica, "Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus" in Neuroscience, 192 (2011):195-204,
https://doi.org/10.1016/j.neuroscience.2011.06.030 . .

TY  - CONF
AU  - Petrovic, S.
AU  - Milošević, Maja
AU  - Drakulić, Dunja R.
AU  - Stanojević, Ivana
AU  - Velickovic, N.
AU  - Horvat, Anica
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6803
C3  - FEBS Journal
T1  - 17beta-estradiol binding to synaptosomal mitochondria isolated from rat brain nucleus caudatus, hippocampus and brain steam
VL  - 276
SP  - 247
EP  - 247
UR  - https://hdl.handle.net/21.15107/rcub_vinar_6803
ER  - 

@conference{
author = "Petrovic, S. and Milošević, Maja and Drakulić, Dunja R. and Stanojević, Ivana and Velickovic, N. and Horvat, Anica",
year = "2009",
journal = "FEBS Journal",
title = "17beta-estradiol binding to synaptosomal mitochondria isolated from rat brain nucleus caudatus, hippocampus and brain steam",
volume = "276",
pages = "247-247",
url = "https://hdl.handle.net/21.15107/rcub_vinar_6803"
}

Petrovic, S., Milošević, M., Drakulić, D. R., Stanojević, I., Velickovic, N.,& Horvat, A.. (2009). 17beta-estradiol binding to synaptosomal mitochondria isolated from rat brain nucleus caudatus, hippocampus and brain steam. in FEBS Journal, 276, 247-247.
https://hdl.handle.net/21.15107/rcub_vinar_6803

Petrovic S, Milošević M, Drakulić DR, Stanojević I, Velickovic N, Horvat A. 17beta-estradiol binding to synaptosomal mitochondria isolated from rat brain nucleus caudatus, hippocampus and brain steam. in FEBS Journal. 2009;276:247-247.
https://hdl.handle.net/21.15107/rcub_vinar_6803 .

Petrovic, S., Milošević, Maja, Drakulić, Dunja R., Stanojević, Ivana, Velickovic, N., Horvat, Anica, "17beta-estradiol binding to synaptosomal mitochondria isolated from rat brain nucleus caudatus, hippocampus and brain steam" in FEBS Journal, 276 (2009):247-247,
https://hdl.handle.net/21.15107/rcub_vinar_6803 .

TY  - CONF
AU  - Drakulić, Dunja R.
AU  - Velickovic, N.
AU  - Milošević, Maja
AU  - Petrovic, S.
AU  - Stanojević, Ivana
AU  - Horvat, Anica
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6804
C3  - FEBS Journal
T1  - Dexamethasone effects on rat hippocampal apoptotic molecules expression
VL  - 276
SP  - 260
EP  - 260
UR  - https://hdl.handle.net/21.15107/rcub_vinar_6804
ER  - 

@conference{
author = "Drakulić, Dunja R. and Velickovic, N. and Milošević, Maja and Petrovic, S. and Stanojević, Ivana and Horvat, Anica",
year = "2009",
journal = "FEBS Journal",
title = "Dexamethasone effects on rat hippocampal apoptotic molecules expression",
volume = "276",
pages = "260-260",
url = "https://hdl.handle.net/21.15107/rcub_vinar_6804"
}

Drakulić, D. R., Velickovic, N., Milošević, M., Petrovic, S., Stanojević, I.,& Horvat, A.. (2009). Dexamethasone effects on rat hippocampal apoptotic molecules expression. in FEBS Journal, 276, 260-260.
https://hdl.handle.net/21.15107/rcub_vinar_6804

Drakulić DR, Velickovic N, Milošević M, Petrovic S, Stanojević I, Horvat A. Dexamethasone effects on rat hippocampal apoptotic molecules expression. in FEBS Journal. 2009;276:260-260.
https://hdl.handle.net/21.15107/rcub_vinar_6804 .

Drakulić, Dunja R., Velickovic, N., Milošević, Maja, Petrovic, S., Stanojević, Ivana, Horvat, Anica, "Dexamethasone effects on rat hippocampal apoptotic molecules expression" in FEBS Journal, 276 (2009):260-260,
https://hdl.handle.net/21.15107/rcub_vinar_6804 .

TY  - CONF
AU  - Velickovic, N.
AU  - Drakulić, Dunja R.
AU  - Petrovic, S.
AU  - Stanojević, Ivana
AU  - Milošević, Maja
AU  - Horvat, Anica
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6805
C3  - FEBS Journal
T1  - Radiation-induced HPA axis activation is associated with up-regulation of pro-inflammatory cytokines in rat brain
VL  - 276
SP  - 269
EP  - 269
UR  - https://hdl.handle.net/21.15107/rcub_vinar_6805
ER  - 

@conference{
author = "Velickovic, N. and Drakulić, Dunja R. and Petrovic, S. and Stanojević, Ivana and Milošević, Maja and Horvat, Anica",
year = "2009",
journal = "FEBS Journal",
title = "Radiation-induced HPA axis activation is associated with up-regulation of pro-inflammatory cytokines in rat brain",
volume = "276",
pages = "269-269",
url = "https://hdl.handle.net/21.15107/rcub_vinar_6805"
}

Velickovic, N., Drakulić, D. R., Petrovic, S., Stanojević, I., Milošević, M.,& Horvat, A.. (2009). Radiation-induced HPA axis activation is associated with up-regulation of pro-inflammatory cytokines in rat brain. in FEBS Journal, 276, 269-269.
https://hdl.handle.net/21.15107/rcub_vinar_6805

Velickovic N, Drakulić DR, Petrovic S, Stanojević I, Milošević M, Horvat A. Radiation-induced HPA axis activation is associated with up-regulation of pro-inflammatory cytokines in rat brain. in FEBS Journal. 2009;276:269-269.
https://hdl.handle.net/21.15107/rcub_vinar_6805 .

Velickovic, N., Drakulić, Dunja R., Petrovic, S., Stanojević, Ivana, Milošević, Maja, Horvat, Anica, "Radiation-induced HPA axis activation is associated with up-regulation of pro-inflammatory cytokines in rat brain" in FEBS Journal, 276 (2009):269-269,
https://hdl.handle.net/21.15107/rcub_vinar_6805 .

TY  - JOUR
AU  - Milošević, Maja
AU  - Petrovic, S.
AU  - Stanojević, Ivana
AU  - Drakulić, Dunja R.
AU  - Velickovic, N.
AU  - Horvat, Anica
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6813
AB  - The aim of this study was to examine in vitro chelators ability to prevent copper-induced inhibition of rat myometrial ecto-ATPase activity. The effects of increasing CuSO(4) concentrations, in the absence and presence of 1 mmol/l EDTA, showed sigmoidal and complete inhibition relative to the control enzyme activity. IC(50) values, 1.15 x 10(-4) and 1.71 x 10(-3) mol/l in the absence and presence of EDTA, respectively, were determined by Hill analysis from experimental curves. According to the results presented in this work, 1 mmol/l EDTA increased by one order of magnitude CuSO(4) concentration for half-maximal inhibition (IC(50)), by decreasing Cu(2+) concentrations, available to form inactive CuATP(2-) complex.
T2  - Russian Journal of Physical Chemistry A
T1  - Effect of EDTA on copper-induced inhibition of rat myometrial ecto-ATPase activity
VL  - 83
IS  - 9
SP  - 1592
EP  - 1595
DO  - 10.1134/S0036024409090313
ER  - 

@article{
author = "Milošević, Maja and Petrovic, S. and Stanojević, Ivana and Drakulić, Dunja R. and Velickovic, N. and Horvat, Anica",
year = "2009",
abstract = "The aim of this study was to examine in vitro chelators ability to prevent copper-induced inhibition of rat myometrial ecto-ATPase activity. The effects of increasing CuSO(4) concentrations, in the absence and presence of 1 mmol/l EDTA, showed sigmoidal and complete inhibition relative to the control enzyme activity. IC(50) values, 1.15 x 10(-4) and 1.71 x 10(-3) mol/l in the absence and presence of EDTA, respectively, were determined by Hill analysis from experimental curves. According to the results presented in this work, 1 mmol/l EDTA increased by one order of magnitude CuSO(4) concentration for half-maximal inhibition (IC(50)), by decreasing Cu(2+) concentrations, available to form inactive CuATP(2-) complex.",
journal = "Russian Journal of Physical Chemistry A",
title = "Effect of EDTA on copper-induced inhibition of rat myometrial ecto-ATPase activity",
volume = "83",
number = "9",
pages = "1592-1595",
doi = "10.1134/S0036024409090313"
}

Milošević, M., Petrovic, S., Stanojević, I., Drakulić, D. R., Velickovic, N.,& Horvat, A.. (2009). Effect of EDTA on copper-induced inhibition of rat myometrial ecto-ATPase activity. in Russian Journal of Physical Chemistry A, 83(9), 1592-1595.
https://doi.org/10.1134/S0036024409090313

Milošević M, Petrovic S, Stanojević I, Drakulić DR, Velickovic N, Horvat A. Effect of EDTA on copper-induced inhibition of rat myometrial ecto-ATPase activity. in Russian Journal of Physical Chemistry A. 2009;83(9):1592-1595.
doi:10.1134/S0036024409090313 .

Milošević, Maja, Petrovic, S., Stanojević, Ivana, Drakulić, Dunja R., Velickovic, N., Horvat, Anica, "Effect of EDTA on copper-induced inhibition of rat myometrial ecto-ATPase activity" in Russian Journal of Physical Chemistry A, 83, no. 9 (2009):1592-1595,
https://doi.org/10.1134/S0036024409090313 . .

TY  - JOUR
AU  - Stanojević, Ivana
AU  - Drakulić, Dunja R.
AU  - Velickovic, N.
AU  - Milošević, Maja
AU  - Petrovic, S.
AU  - Horvat, Anica
PY  - 2009
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/6814
AB  - Cell membrane is highly sensitive to irradiation which, acting directly or indirectly, may disturb functions of constitutive proteins including membrane enzymes. Plasma membrane surface-located enzyme chain of ecto-nucleotide triphospho diphosphohydrolases (NTPDases) and 5-nucleotidase are involved in termination of cell purinergic signalization by hydrolyzing extracellular, excitatory adenosine triphosphate (ATP), as well as nucleotide di-, and mono-phosphate (ADP and AMP) to neuroprotective adenosine. Extracellular ATP, ADP, and AMP hydrolyzes were examined in purified synaptic plasma membranes after whole-body acute irradiation. All measurements were done 24 h after irradiation of developing (15-, 30-day-old) and adult (90-day-old) rats with low (50 cGy) and high (2 Gy) dose of gamma-rays. Both, high and low doses inhibited nucleotide hydrolyses in 15-day-old rats; in 30-day-old rats low dose of radiation inhibited ADP and AMP hydrolyses while high dose inhibited only ATP hydrolyse. In adult rats high dose induced no effects, while low dose stimulated nucleotides hydrolyses. According to obtained results it was concluded that ecto-nucleotidases of young rats are more sensitive to irradiation, since even low dose induces inhibition of ecto-nucleotidases activities. Ionizing radiation, by decreasing brain nucleotide hydrolyses in developing rats, induces accumulation of ATP and decreases production of adenosine in synaptic cleft which could be neurocytotoxic. On the contrary, in adult rats low dose of radiation stimulates NTPDase and 5-nucleotidase activity and protective adenosine production which indicates protective and adaptive mechanisms developed in adult brain neuronal cells.
T2  - Russian Journal of Physical Chemistry A
T1  - Effects of acute gamma-irradiation on extracellular adenine nucleotide hydrolysis in developing rat brain
VL  - 83
IS  - 9
SP  - 1596
EP  - 1601
DO  - 10.1134/S0036024409090325
ER  - 

@article{
author = "Stanojević, Ivana and Drakulić, Dunja R. and Velickovic, N. and Milošević, Maja and Petrovic, S. and Horvat, Anica",
year = "2009",
abstract = "Cell membrane is highly sensitive to irradiation which, acting directly or indirectly, may disturb functions of constitutive proteins including membrane enzymes. Plasma membrane surface-located enzyme chain of ecto-nucleotide triphospho diphosphohydrolases (NTPDases) and 5-nucleotidase are involved in termination of cell purinergic signalization by hydrolyzing extracellular, excitatory adenosine triphosphate (ATP), as well as nucleotide di-, and mono-phosphate (ADP and AMP) to neuroprotective adenosine. Extracellular ATP, ADP, and AMP hydrolyzes were examined in purified synaptic plasma membranes after whole-body acute irradiation. All measurements were done 24 h after irradiation of developing (15-, 30-day-old) and adult (90-day-old) rats with low (50 cGy) and high (2 Gy) dose of gamma-rays. Both, high and low doses inhibited nucleotide hydrolyses in 15-day-old rats; in 30-day-old rats low dose of radiation inhibited ADP and AMP hydrolyses while high dose inhibited only ATP hydrolyse. In adult rats high dose induced no effects, while low dose stimulated nucleotides hydrolyses. According to obtained results it was concluded that ecto-nucleotidases of young rats are more sensitive to irradiation, since even low dose induces inhibition of ecto-nucleotidases activities. Ionizing radiation, by decreasing brain nucleotide hydrolyses in developing rats, induces accumulation of ATP and decreases production of adenosine in synaptic cleft which could be neurocytotoxic. On the contrary, in adult rats low dose of radiation stimulates NTPDase and 5-nucleotidase activity and protective adenosine production which indicates protective and adaptive mechanisms developed in adult brain neuronal cells.",
journal = "Russian Journal of Physical Chemistry A",
title = "Effects of acute gamma-irradiation on extracellular adenine nucleotide hydrolysis in developing rat brain",
volume = "83",
number = "9",
pages = "1596-1601",
doi = "10.1134/S0036024409090325"
}

Stanojević, I., Drakulić, D. R., Velickovic, N., Milošević, M., Petrovic, S.,& Horvat, A.. (2009). Effects of acute gamma-irradiation on extracellular adenine nucleotide hydrolysis in developing rat brain. in Russian Journal of Physical Chemistry A, 83(9), 1596-1601.
https://doi.org/10.1134/S0036024409090325

Stanojević I, Drakulić DR, Velickovic N, Milošević M, Petrovic S, Horvat A. Effects of acute gamma-irradiation on extracellular adenine nucleotide hydrolysis in developing rat brain. in Russian Journal of Physical Chemistry A. 2009;83(9):1596-1601.
doi:10.1134/S0036024409090325 .

Stanojević, Ivana, Drakulić, Dunja R., Velickovic, N., Milošević, Maja, Petrovic, S., Horvat, Anica, "Effects of acute gamma-irradiation on extracellular adenine nucleotide hydrolysis in developing rat brain" in Russian Journal of Physical Chemistry A, 83, no. 9 (2009):1596-1601,
https://doi.org/10.1134/S0036024409090325 . .