Oxidative stress plays a central role in the pathophysiology of type 2 diabetes mellitus (T2DM), contributing to vascular complications such as diabetic retinopathy. Increased free radical production in T2DM arises from nonenzymatic glycosylation of proteins, glucose auto-oxidation, and enhanced glucose metabolism through the sorbitol pathway. These processes, combined with poor glycemic control, lead to depletion of endogenous antioxidant defenses. Paraoxonase 1 (PON1), a calcium-dependent esterase primarily bound to high-density lipoprotein (HDL), serves as a critical antioxidant enzyme by hydrolyzing lipid peroxides in oxidized lipoproteins. Reduced PON1 activity has been observed in patients with diabetes and other conditions characterized by elevated oxidative stress. Malondialdehyde (MDA), a major product of lipid peroxidation, is a widely recognized biomarker of oxidative damage. This study evaluated basal and stimulated PON1 activities alongside serum MDA levels in patients with diabetic retinopathy, aiming to elucidate the relationship between antioxidant capacity and oxidative damage in this population. Understanding these biochemical markers may provide insights into the oxidative mechanisms underlying diabetic complications and inform potential therapeutic strategies targeting antioxidant pathways
Yılmaz et al. (Sun,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: