Velicković, Nataša

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orcid::0000-0003-3604-5836
  • Velicković, Nataša (2)
  • Veličković, Nataša (2)

Author's Bibliography

Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats

Paunović, Marija; Milošević, Maja; Mitrović-Ajtić, Olivera; Veličković, Nataša; Mićić, Bojana; Nedić, Olgica; Todorović, Vanja; Vučić, Vesna; Petrović, Snježana

(Elsevier, 2024)

TY  - JOUR
AU  - Paunović, Marija
AU  - Milošević, Maja
AU  - Mitrović-Ajtić, Olivera
AU  - Veličković, Nataša
AU  - Mićić, Bojana
AU  - Nedić, Olgica
AU  - Todorović, Vanja
AU  - Vučić, Vesna
AU  - Petrović, Snježana
PY  - 2024
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/1476
AB  - Diets high in fat and sugar lead to metabolic syndrome (MetS) and related chronic diseases. We investigated the effects of commercially available, cold-pressed polyphenol-rich black currant (BC) and cornelian cherry (CC) juices on the prevention of MetS in Wistar rats induced by a 10-weeks high-fat high-fructose (HFF) diet. Juice consumption, either BC or CC, with a HFF diet resulted in lower serum triglycerides compared to only the HFF consumption. Both juices also mitigated the effects of HFF on the liver, pancreas, and adipose tissue, by preserving liver and pancreas histomorphology and reducing visceral fat and adipocyte size. Furthermore, supplementation with both juices reduced glucagon and up-regulated insulin expression in the pancreas of the rats on the HFF diet, whereas the BC also showed improved glucose regulation. BC juice also reduced the expression of IL-6 and hepatic inflammation compared to the group only on HFF diet. Both juices, especially BC, could be a convenient solution for the prevention of MetS in humans.
PB  - Elsevier
T2  - Heliyon
T1  - Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats
IS  - 7
SP  - e27709
VL  - 10
DO  - 10.1016/j.heliyon.2024.e27709
ER  - 
@article{
author = "Paunović, Marija and Milošević, Maja and Mitrović-Ajtić, Olivera and Veličković, Nataša and Mićić, Bojana and Nedić, Olgica and Todorović, Vanja and Vučić, Vesna and Petrović, Snježana",
year = "2024",
abstract = "Diets high in fat and sugar lead to metabolic syndrome (MetS) and related chronic diseases. We investigated the effects of commercially available, cold-pressed polyphenol-rich black currant (BC) and cornelian cherry (CC) juices on the prevention of MetS in Wistar rats induced by a 10-weeks high-fat high-fructose (HFF) diet. Juice consumption, either BC or CC, with a HFF diet resulted in lower serum triglycerides compared to only the HFF consumption. Both juices also mitigated the effects of HFF on the liver, pancreas, and adipose tissue, by preserving liver and pancreas histomorphology and reducing visceral fat and adipocyte size. Furthermore, supplementation with both juices reduced glucagon and up-regulated insulin expression in the pancreas of the rats on the HFF diet, whereas the BC also showed improved glucose regulation. BC juice also reduced the expression of IL-6 and hepatic inflammation compared to the group only on HFF diet. Both juices, especially BC, could be a convenient solution for the prevention of MetS in humans.",
publisher = "Elsevier",
journal = "Heliyon",
title = "Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats",
number = "7",
pages = "e27709",
volume = "10",
doi = "10.1016/j.heliyon.2024.e27709"
}
Paunović, M., Milošević, M., Mitrović-Ajtić, O., Veličković, N., Mićić, B., Nedić, O., Todorović, V., Vučić, V.,& Petrović, S.. (2024). Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats. in Heliyon
Elsevier., 10(7), e27709.
https://doi.org/10.1016/j.heliyon.2024.e27709
Paunović M, Milošević M, Mitrović-Ajtić O, Veličković N, Mićić B, Nedić O, Todorović V, Vučić V, Petrović S. Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats. in Heliyon. 2024;10(7):e27709.
doi:10.1016/j.heliyon.2024.e27709 .
Paunović, Marija, Milošević, Maja, Mitrović-Ajtić, Olivera, Veličković, Nataša, Mićić, Bojana, Nedić, Olgica, Todorović, Vanja, Vučić, Vesna, Petrović, Snježana, "Polyphenol-rich black currant and cornelian cherry juices ameliorate metabolic syndrome induced by a high-fat high-fructose diet in Wistar rats" in Heliyon, 10, no. 7 (2024):e27709,
https://doi.org/10.1016/j.heliyon.2024.e27709 . .

Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress

Velicković, Nataša; Teofilović, Ana; Ilić, Dragana; Đorđević, Ana; Vojnović-Milutinović, Danijela; Petrović, Snježana; Preitner, Frederic; Tappy, Luc; Matić, Gordana

(Springer Heidelberg, Heidelberg, 2019)

TY  - JOUR
AU  - Velicković, Nataša
AU  - Teofilović, Ana
AU  - Ilić, Dragana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Petrović, Snježana
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2019
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/913
AB  - Purpose High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. Methods In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose diet led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. Conclusion High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.
PB  - Springer Heidelberg, Heidelberg
T2  - European Journal of Nutrition
T1  - Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress
EP  - 1845
IS  - 5
SP  - 1829
VL  - 58
DO  - 10.1007/s00394-018-1730-1
ER  - 
@article{
author = "Velicković, Nataša and Teofilović, Ana and Ilić, Dragana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Petrović, Snježana and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2019",
abstract = "Purpose High-fructose consumption and chronic stress are both associated with metabolic inflammation and insulin resistance. Recently, disturbed activity of energy sensor AMP-activated protein kinase (AMPK) was recognized as mediator between nutrient-induced stress and inflammation. Thus, we analyzed the effects of high-fructose diet, alone or in combination with chronic stress, on glucose homeostasis, inflammation and expression of energy sensing proteins in the rat liver. Methods In male Wistar rats exposed to 9-week 20% fructose diet and/or 4-week chronic unpredictable stress we measured plasma and hepatic corticosterone level, indicators of glucose homeostasis and lipid metabolism, hepatic inflammation (pro- and anti-inflammatory cytokine levels, Toll-like receptor 4, NLRP3, activation of NF kappa B, JNK and ERK pathways) and levels of energy-sensing proteins AMPK, SIRT1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha). Results High-fructose diet led to glucose intolerance, activation of NF kappa B and JNK pathways and increased intrahepatic IL-1 beta, TNF alpha and inhibitory phosphorylation of insulin receptor substrate 1 on Ser(307). It also decreased phospho-AMPK/AMPK ratio and increased SIRT1 expression. Stress alone increased plasma and hepatic corticosterone but did not influence glucose tolerance, nor hepatic inflammatory or energy-sensing proteins. After the combined treatment, hepatic corticosterone was increased, glucose tolerance remained preserved, while hepatic inflammation was partially prevented despite decreased AMPK activity. Conclusion High-fructose diet resulted in glucose intolerance, hepatic inflammation, decreased AMPK activity and reduced insulin sensitivity. Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids.",
publisher = "Springer Heidelberg, Heidelberg",
journal = "European Journal of Nutrition",
title = "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress",
pages = "1845-1829",
number = "5",
volume = "58",
doi = "10.1007/s00394-018-1730-1"
}
Velicković, N., Teofilović, A., Ilić, D., Đorđević, A., Vojnović-Milutinović, D., Petrović, S., Preitner, F., Tappy, L.,& Matić, G.. (2019). Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress. in European Journal of Nutrition
Springer Heidelberg, Heidelberg., 58(5), 1829-1845.
https://doi.org/10.1007/s00394-018-1730-1
Velicković N, Teofilović A, Ilić D, Đorđević A, Vojnović-Milutinović D, Petrović S, Preitner F, Tappy L, Matić G. Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress. in European Journal of Nutrition. 2019;58(5):1829-1845.
doi:10.1007/s00394-018-1730-1 .
Velicković, Nataša, Teofilović, Ana, Ilić, Dragana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Petrović, Snježana, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress" in European Journal of Nutrition, 58, no. 5 (2019):1829-1845,
https://doi.org/10.1007/s00394-018-1730-1 . .
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Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet

Bursać, Biljana; Đorđević, Ana; Veličković, Nataša; Vojnović-Milutinović, Danijela; Petrović, Snježana; Teofilović, Ana; Gligorovska, Ljupka; Preitner, Frédéric; Tappy, Luc; Matić, Gordana

(Elsevier Ireland Ltd, Clare, 2018)

TY  - JOUR
AU  - Bursać, Biljana
AU  - Đorđević, Ana
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Petrović, Snježana
AU  - Teofilović, Ana
AU  - Gligorovska, Ljupka
AU  - Preitner, Frédéric
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/860
AB  - Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Delta 9 desaturase activity. The results showed that fructose diet increased blood triglycerides and Delta 9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose diet was associated with marked stimulation of fatty acid synthase and acetylCoA carboxylase mRNA level and with increased 11 beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction.
PB  - Elsevier Ireland Ltd, Clare
T2  - Molecular & Cellular Endocrinology
T1  - Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet
EP  - 118
SP  - 110
VL  - 476
DO  - 10.1016/j.mce.2018.04.015
ER  - 
@article{
author = "Bursać, Biljana and Đorđević, Ana and Veličković, Nataša and Vojnović-Milutinović, Danijela and Petrović, Snježana and Teofilović, Ana and Gligorovska, Ljupka and Preitner, Frédéric and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Delta 9 desaturase activity. The results showed that fructose diet increased blood triglycerides and Delta 9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose diet was associated with marked stimulation of fatty acid synthase and acetylCoA carboxylase mRNA level and with increased 11 beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction.",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Molecular & Cellular Endocrinology",
title = "Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet",
pages = "118-110",
volume = "476",
doi = "10.1016/j.mce.2018.04.015"
}
Bursać, B., Đorđević, A., Veličković, N., Vojnović-Milutinović, D., Petrović, S., Teofilović, A., Gligorovska, L., Preitner, F., Tappy, L.,& Matić, G.. (2018). Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet. in Molecular & Cellular Endocrinology
Elsevier Ireland Ltd, Clare., 476, 110-118.
https://doi.org/10.1016/j.mce.2018.04.015
Bursać B, Đorđević A, Veličković N, Vojnović-Milutinović D, Petrović S, Teofilović A, Gligorovska L, Preitner F, Tappy L, Matić G. Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet. in Molecular & Cellular Endocrinology. 2018;476:110-118.
doi:10.1016/j.mce.2018.04.015 .
Bursać, Biljana, Đorđević, Ana, Veličković, Nataša, Vojnović-Milutinović, Danijela, Petrović, Snježana, Teofilović, Ana, Gligorovska, Ljupka, Preitner, Frédéric, Tappy, Luc, Matić, Gordana, "Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with high-fructose diet" in Molecular & Cellular Endocrinology, 476 (2018):110-118,
https://doi.org/10.1016/j.mce.2018.04.015 . .
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Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem

Petrović, Snježana; Milošević, Maja; Ristić-Medić, Danijela; Velicković, Nataša; Drakulić, Dunja; Grković, Ivana; Horvat, Anica

(Tubitak Scientific & Technical Research Council Turkey, Ankara, 2015)

TY  - JOUR
AU  - Petrović, Snježana
AU  - Milošević, Maja
AU  - Ristić-Medić, Danijela
AU  - Velicković, Nataša
AU  - Drakulić, Dunja
AU  - Grković, Ivana
AU  - Horvat, Anica
PY  - 2015
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/662
AB  - Our earlier studies found that in vitro estradiol modulates mitochondrial Ca2+ transport in discrete brain regions. The present study examined the role of estradiol receptors (ERs) in estradiol-induced inhibition of Ca2+ efflux from synaptosomal mitochondria isolated from rat caudate nuclei and brain stems. Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for Ca2+ transport monitoring. The results revealed that in the presence of ER antagonist 7 alpha, 17 beta-[9[(4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux was more than 60% decreased, suggesting the involvement of ER in this mode of estradiol neuromodulatory action. When particular contributions of ER alpha and ER beta were tested, it was found that ER beta agonist 2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+ efflux more than 20%, while the inhibition with ER alpha agonist 4,4', 4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was about 10%, both compared to the control. Both agonists demonstrated attenuation of Ca2+ efflux decrease in the presence of mitochondrial Na+/Ca2+ exchanger antagonist 7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one (10 mu mol/L), showing interference with the inhibitory action of that agent. Our results strongly indicate ERs as the mediators of estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate nucleus and brain stem synaptosomes.
PB  - Tubitak Scientific & Technical Research Council Turkey, Ankara
T2  - Turkish Journal of Biology
T1  - Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem
EP  - 334
IS  - 2
SP  - 328
VL  - 39
DO  - 10.3906/biy-1408-62
ER  - 
@article{
author = "Petrović, Snježana and Milošević, Maja and Ristić-Medić, Danijela and Velicković, Nataša and Drakulić, Dunja and Grković, Ivana and Horvat, Anica",
year = "2015",
abstract = "Our earlier studies found that in vitro estradiol modulates mitochondrial Ca2+ transport in discrete brain regions. The present study examined the role of estradiol receptors (ERs) in estradiol-induced inhibition of Ca2+ efflux from synaptosomal mitochondria isolated from rat caudate nuclei and brain stems. Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for Ca2+ transport monitoring. The results revealed that in the presence of ER antagonist 7 alpha, 17 beta-[9[(4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux was more than 60% decreased, suggesting the involvement of ER in this mode of estradiol neuromodulatory action. When particular contributions of ER alpha and ER beta were tested, it was found that ER beta agonist 2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+ efflux more than 20%, while the inhibition with ER alpha agonist 4,4', 4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was about 10%, both compared to the control. Both agonists demonstrated attenuation of Ca2+ efflux decrease in the presence of mitochondrial Na+/Ca2+ exchanger antagonist 7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one (10 mu mol/L), showing interference with the inhibitory action of that agent. Our results strongly indicate ERs as the mediators of estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate nucleus and brain stem synaptosomes.",
publisher = "Tubitak Scientific & Technical Research Council Turkey, Ankara",
journal = "Turkish Journal of Biology",
title = "Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem",
pages = "334-328",
number = "2",
volume = "39",
doi = "10.3906/biy-1408-62"
}
Petrović, S., Milošević, M., Ristić-Medić, D., Velicković, N., Drakulić, D., Grković, I.,& Horvat, A.. (2015). Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology
Tubitak Scientific & Technical Research Council Turkey, Ankara., 39(2), 328-334.
https://doi.org/10.3906/biy-1408-62
Petrović S, Milošević M, Ristić-Medić D, Velicković N, Drakulić D, Grković I, Horvat A. Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology. 2015;39(2):328-334.
doi:10.3906/biy-1408-62 .
Petrović, Snježana, Milošević, Maja, Ristić-Medić, Danijela, Velicković, Nataša, Drakulić, Dunja, Grković, Ivana, Horvat, Anica, "Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem" in Turkish Journal of Biology, 39, no. 2 (2015):328-334,
https://doi.org/10.3906/biy-1408-62 . .