Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro.

Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders and diabetes. The main objective of this investigation was to find out whether peripheral blood mononuclear cells (PBMCs) are more prone to DNA damage by triiodothyronine (T3) (0.1, 1 and 10 µM) at various stages of progression through diabetes (obese, prediabetics, and type 2 diabetes mellitus-T2DM persons). In addition, some biochemical parameters of oxidative stress (catalase-CAT, thiobarbituric acid reactive substances-TBARS) and lactate dehydrogenase (LDH) were evaluated. PBMCs from prediabetic and diabetic patients exhibited increased sensitivity for T3 regarding elevated level of DNA damage, inhibition of catalase, and increase of TBARS and LDH. PBMCs from obese patients reacted in the same manner, except for DNA damage. The results of this study should contribute to a better understanding of the role of thyroid hormones in the progression of T2DM.

Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to adrenaline in vitro.

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.