Metabolic syndrome (MetS) is a multifactorial disorder characterized by central obesity, insulin resistance, dyslipidemia, elevated blood pressure, and chronic low-grade inflammation. Oxidative stress is considered an important mechanism linking these metabolic abnormalities to cardiovascular disease and type 2 diabetes mellitus. It occurs when reactive oxygen species (ROS) production exceeds the capacity of endogenous antioxidant defenses. In MetS, excessive nutrient availability, adipose tissue dysfunction, hyperglycemia, elevated free fatty acids, mitochondrial dysfunction, and activation of ROS-producing enzymes contribute to increased oxidative burden. Persistent oxidative stress promotes lipid, protein, and DNA damage, endothelial dysfunction, inflammation, and impaired insulin signaling. At the same time, disruption of enzymatic and non-enzymatic antioxidant defenses further compromises redox homeostasis. This review summarizes the major mechanisms of oxidative stress and antioxidant imbalance in MetS, focusing on mitochondrial ROS production, inflammation, insulin resistance, endothelial dysfunction, and oxidative stress biomarkers. The potential role of antioxidant defenses and lifestyle-based interventions in restoring redox balance is also discussed..
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Sherzod qizi Toirova Shahrizoda (2026) studied this question.
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