Djelić Ninoslav, Radaković Milena, Borozan Sunčica, Dimirijević-Srećković Vesna, Pajović Nevena, Vejnović Branislav, Borozan Nevena, Bankoglu Ezgi Eylül, Stopper Helga, Stanimirović Zoran
Department of Biology, Faculty of Veterinary Medicine, University of Belgrade, Serbia.
Department of Chemistry, Faculty of Veterinary Medicine, University of Belgrade, Serbia.
Mutat Res Genet Toxicol Environ Mutagen. 2019 Jul;843:81-89. doi: 10.1016/j.mrgentox.2019.01.013. Epub 2019 Jan 24.
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.
糖尿病是主要的健康问题之一，在发达国家尤为如此。一些激素，如应激激素肾上腺素，可诱导活性氧（ROS）产生，可能会使糖尿病病情恶化。因此，本研究的主要目的是探究与肥胖、糖尿病前期和糖尿病患者的外周血单个核细胞（PBMC）相比，正常人的PBMC在肾上腺素（0.1、1和10 μM）诱导下的DNA损伤是否更少。此外，还监测了氧化应激的生化参数（丙二醛、过氧化氢酶）和乳酸脱氢酶。结果发现，较高浓度的肾上腺素（1和10 μM）在肥胖、糖尿病前期和糖尿病组中诱导了DNA损伤。在健康个体中，只有最高浓度的肾上腺素导致DNA损伤显著增加。总之，总彗星试验评分（TCS）比较显示各组之间存在显著差异，肾上腺素对DNA的损伤作用在糖尿病患者中最为明显。生化分析结果还表明，肾上腺素在糖尿病个体中发挥的作用最为明显，表现为氧化应激参数的显著变化。总之，所得结果表明糖尿病患者对肾上腺素的遗传毒性作用更敏感，这种作用可能是由于糖尿病进展各阶段抗氧化防御机制下降所致。因此，这些结果有助于更好地理解内分泌因素在细胞生物分子损伤中的作用，这可能有助于寻找新的治疗方法和改变生活方式，以降低糖尿病并发症的发生可能性。
