A review of domestic and foreign studies on the role of oxidative stress in the pathogenesis of the metabolic syndrome is presented. It is noted that metabolic syndrome is one of the factors determining cardiovascular risk since oxidative stress results from excessive accumulation of lipid and carbohydrate metabolism products. Various aspects of the effect of reactive oxygen and nitrogen forms and other free radicals on oxidative stress development in disorders comprising the metabolic syndrome complex are addressed. Thus, the mechanisms of chronic inflammation due to excessive secretion of proinflammatory cytokines and adipokines, activation of the transcription factor NF-κB, and antioxidant system dysfunction in obesity are described. Some mechanisms of adipokines’ effect on oxidative stress are considered individually: leptin, adiponectin, chimerin, and omentin type 1. In addition, the review describes polyol pathway activation variants and diacyl-glycerol-protein kinase C-signaling pathway of oxidative stress and mitochondrial dysfunction resulting in excess free radical production in insulin resistance, diabetes mellitus, and its macro- and microvascular complications.