TY  - JOUR
AU  - Đelić, Ninoslav
AU  - Radaković, Milena
AU  - Borozan, Sunčica
AU  - Dimirijević-Srecković, Vesna
AU  - Pajović, Nevena
AU  - Vejnović, Branislav
AU  - Borozan, Nevena
AU  - Bankoglu, Ezgi Eylul
AU  - Stopper, Helga
AU  - Stanimirović, Zoran
PY  - 2019
UR  - https://vet-erinar.vet.bg.ac.rs/handle/123456789/1780
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 mu M) 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 mu M) 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, Amsterdam
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 adrenaline 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-Srecković, Vesna and Pajović, Nevena and Vejnović, Branislav and Borozan, Nevena and Bankoglu, Ezgi Eylul 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 mu M) 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 mu M) 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, Amsterdam",
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 adrenaline in vitro",
volume = "843",
pages = "81-89",
doi = "10.1016/j.mrgentox.2019.01.013"
}

Đelić, N., Radaković, M., Borozan, S., Dimirijević-Srecković, 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 adrenaline in vitro. in Mutation Research-Genetic Toxicology and Environmental Mutagenesis
Elsevier, Amsterdam., 843, 81-89.
https://doi.org/10.1016/j.mrgentox.2019.01.013

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