TY  - JOUR
AU  - Đelić, Ninoslav
AU  - Radaković, Milena
AU  - Borozan, Sunčica
AU  - Dimirijević-Srećković, Vesna
AU  - Pajović, Nevena
AU  - Vejnović, Branislav
AU  - Borozan, Nevena
AU  - Bankoglu, Ezgi Eylül
AU  - Stopper, Helga
AU  - Stanimirović, Zoran
PY  - 2019
UR  - https://vet-erinar.vet.bg.ac.rs/handle/123456789/2546
AB  - Diabetes represents one of the major health concerns, especially in developed countries. Some hormones such as
the stress hormone adrenaline can induce reactive oxygen species (ROS) and may worsen the diabetes.
Therefore, the main aim of the investigation was to find out whether peripheral blood mononuclear cells
(PBMCs) from normal persons have less DNA damage induced by adrenaline (0.1, 1 and 10 μM) in comparison to
PBMCs from obese, prediabetic and diabetic patients. Also, the biochemical parameters of oxidative stress
(TBARS, catalase) and lactate dehydrogenase were monitored. It was observed that higher concentrations of
adrenaline (1 and 10 μM) induced DNA damage in the obese, prediabetic and diabetic groups. In healthy individuals only the highest concentration of adrenaline caused significant increase in the DNA damage. In
summary, total comet score (TCS) comparison has shown significant differences between groups, and DNA
damaging effects of adrenaline were most evident in diabetic patients. The results of the biochemical analysis
also demonstrate that adrenaline exerts most obvious effects in diabetic individuals which is manifested as
significant change of parameters of oxidative stress. In summary, the obtained results demonstrated that diabetics are more sensitive to genotoxic effects of adrenaline and this effect probably resulted from decreased
antioxidative defence mechanisms in various stages of progression through diabetes. Therefore, these results
could contribute to a better understanding of a role of endocrine factors to damage of cellular biomolecules
which could be useful in finding novel therapeutic approaches and lifestyle changes with an aim to lower the
possibility of diabetes complications.
PB  - Elsevier
T2  - Mutation Research: Genetic Toxicology and Environmental Mutagenesis
T1  - Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro
VL  - 843
SP  - 81
EP  - 89
DO  - 10.1016/j.mrgentox.2019.01.013
ER  - 

@article{
author = "Đelić, Ninoslav and Radaković, Milena and Borozan, Sunčica and Dimirijević-Srećković, Vesna and Pajović, Nevena and Vejnović, Branislav and Borozan, Nevena and Bankoglu, Ezgi Eylül and Stopper, Helga and Stanimirović, Zoran",
year = "2019",
abstract = "Diabetes represents one of the major health concerns, especially in developed countries. Some hormones such as
the stress hormone adrenaline can induce reactive oxygen species (ROS) and may worsen the diabetes.
Therefore, the main aim of the investigation was to find out whether peripheral blood mononuclear cells
(PBMCs) from normal persons have less DNA damage induced by adrenaline (0.1, 1 and 10 μM) in comparison to
PBMCs from obese, prediabetic and diabetic patients. Also, the biochemical parameters of oxidative stress
(TBARS, catalase) and lactate dehydrogenase were monitored. It was observed that higher concentrations of
adrenaline (1 and 10 μM) induced DNA damage in the obese, prediabetic and diabetic groups. In healthy individuals only the highest concentration of adrenaline caused significant increase in the DNA damage. In
summary, total comet score (TCS) comparison has shown significant differences between groups, and DNA
damaging effects of adrenaline were most evident in diabetic patients. The results of the biochemical analysis
also demonstrate that adrenaline exerts most obvious effects in diabetic individuals which is manifested as
significant change of parameters of oxidative stress. In summary, the obtained results demonstrated that diabetics are more sensitive to genotoxic effects of adrenaline and this effect probably resulted from decreased
antioxidative defence mechanisms in various stages of progression through diabetes. Therefore, these results
could contribute to a better understanding of a role of endocrine factors to damage of cellular biomolecules
which could be useful in finding novel therapeutic approaches and lifestyle changes with an aim to lower the
possibility of diabetes complications.",
publisher = "Elsevier",
journal = "Mutation Research: Genetic Toxicology and Environmental Mutagenesis",
title = "Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro",
volume = "843",
pages = "81-89",
doi = "10.1016/j.mrgentox.2019.01.013"
}

Đelić, N., Radaković, M., Borozan, S., Dimirijević-Srećković, V., Pajović, N., Vejnović, B., Borozan, N., Bankoglu, E. E., Stopper, H.,& Stanimirović, Z.. (2019). Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro. in Mutation Research: Genetic Toxicology and Environmental Mutagenesis
Elsevier., 843, 81-89.
https://doi.org/10.1016/j.mrgentox.2019.01.013

Đelić N, Radaković M, Borozan S, Dimirijević-Srećković V, Pajović N, Vejnović B, Borozan N, Bankoglu EE, Stopper H, Stanimirović Z. Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro. in Mutation Research: Genetic Toxicology and Environmental Mutagenesis. 2019;843:81-89.
doi:10.1016/j.mrgentox.2019.01.013 .

Đelić, Ninoslav, Radaković, Milena, Borozan, Sunčica, Dimirijević-Srećković, Vesna, Pajović, Nevena, Vejnović, Branislav, Borozan, Nevena, Bankoglu, Ezgi Eylül, Stopper, Helga, Stanimirović, Zoran, "Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro" in Mutation Research: Genetic Toxicology and Environmental Mutagenesis, 843 (2019):81-89,
https://doi.org/10.1016/j.mrgentox.2019.01.013 . .