4.7 Article

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

期刊

出版社

MDPI
DOI: 10.3390/ijms23169072

关键词

diabetes; oxidative stress; DNA damage; lymphocytes; thyroid hormone

资金

  1. DAAD
  2. Serbian Ministry of Education, Science and Technological Development [451-03-68/2022-14/200143]
  3. COST action hCOMET [CA 15132]

向作者/读者索取更多资源

This study investigated the impact of triiodothyronine (T-3) on DNA damage and oxidative stress in peripheral blood mononuclear cells (PBMCs) at different stages of diabetes. The results showed that prediabetic and diabetic patients were more sensitive to T-3, exhibiting elevated DNA damage, inhibition of catalase, and increased levels of TBARS and LDH. Obese patients showed similar responses except for DNA damage.
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 (T-3) (0.1, 1 and 10 mu M) 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 T-3 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.

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