The review presents modern views about the role of oxidative stress reactions in the pathogenesis of types 1 and 2 diabetes mellitus and their complications based on the analysis of experimental and clinical studies. The sources of increased ROS generation in diabetes are specified, including the main pathways of altered glucose metabolism, oxidative damage to pancreatic β-cells, and endothelial dysfunction. The relationship between oxidative stress, carbonyl stress, and inflammation is described. The significance of oxidative stress reactions associated with hyperglycemia is considered in the context of the “metabolic memory” phenomenon. The results of our studies demonstrated significant ethnic and age-related variability of the LPO—antioxidant defense system parameters in patients with diabetes mellitus, which should be considered during complex therapy of the disease. Numerous studies of the effectiveness of antioxidants in diabetes mellitus of both types convincingly proved that antioxidants should be a part of the therapeutic process. Modern therapeutic strategies in the treatment of diabetes mellitus are aimed at developing new methods of personalized antioxidant therapy, including ROS sources targeting combined with new ways of antioxidant delivery.

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Specific features of LPO processes and antioxidant defense were studied in patients with polycystic ovarian syndrome (PCOS) and infertility. Changes in LPO processes in patients with PCOS were compensatory, which manifested in increased α-tocopherol and retinol concentrations and moderate decrease in superoxide dismutase activity. Intensification of prooxidant processes was found in the group of patients with infertility without PCOS. The observed changes necessitate differentiated approach to the treatment of these patients.

Here we performed individual evaluation of the oxidative stress index that serves as an integral criterion for the balance of LPO-antioxidant defense system in women with endocrine pathology (type 1 diabetes mellitus and infertility with hyperprolactinemia). The state of the LPO-antioxidant defense system was estimated from blood levels of LPO substrates with conjugated double bonds, conjugated dienes, ketodienes, conjugated trienes, thiobarbituric acid-reactive substances, retinol, α-tocopherol, reduced and oxidized glutathione, and SOD activity. The use of this oxidative stress index allowed us to diagnose oxidative stress in female patients with endocrine pathology.