Association of oxidative stress markers and trace element imbalance with glycemic control in type 2 diabetes mellitus

Background. An imbalance in favor of oxidants (prooxidants) over antioxidants, which disrupts redox signaling and causes molecular damage in cells, is known as oxidative stress. Oxidants, often reactive oxygen species and reactive nitrogen species, are highly reactive molecules produced both endogenously (e.g., mitochondria) and from external sources (e.g., pollution, radiation), which can damage lipids, proteins, DNA, and other cellular components. The purpose of the study was to assess and compare fasting blood glucose, glycated hemoglobin, malondialdehyde, reduced glutathione, zinc (Zn), copper (Cu), selenium (Se), iron, total cholesterol, low-density lipoprotein, high-density lipoprotein (HDL), and triglycerides in patients with type 2 diabetes mallitus (T2DM) and healthy controls. Materials and methods. A total of 200 participants were recruited and allocated into two groups: 100 patients diagnosed with T2DM and 100 apparently healthy control subjects. The duration of T2DM and metformin therapy ranged from 1 to 3 years. All diabetic patients were receiving metformin at a standardized dose of 500 mg twice daily. Individuals with a history of smoking were excluded to avoid potential confounding effects on oxidative stress and biochemical parameters. Results. The analysis demonstrated that patients with T2DM exhibited significantly higher levels of fasting blood glucose, glycated hemoglobin, malondialdehyde, Cu, total cholesterol, low-density lipoprotein and triglycerides compared to healthy controls (P ≤ 0.05). In contrast, levels of reduced glutathione, Zn, Se, and HDL were significantly lower in the T2DM group. No statistically significant difference was observed in serum iron levels between patients and controls. An imbalance in trace elements that regulate oxidative stress is suggested by the rise in Cu and decrease in Zn and Se; Cu tends to enhance oxidative processes while Zn and Se function as antioxidants; thus, their loss may worsen oxidative damage. Conclusions. The results show that considerable changes in glycemic indices, lipid profiles, oxidative stress markers, and trace element status are linked to T2DM. Reduced antioxidant levels and an increase in oxidative stress indicators point to a possible role for oxidative imbalance in the pathogenesis of T2DM. Furthermore, sex-related variations in iron and HDL levels might be a reflection of underlying biological differences that need more research.