Oxidative stress and antioxidant defense system in atherosclerosis and diabetes mellitus type 2

Relevance. Cardiovascular diseases are the leading cause of death, and the current therapy is imperfect, as it has many side effects, and is ineffective for about a third of patients. In this review, we consider the role of oxidative stress in diseases of atherosclerotic genesis, such as type 2 diabetes mellitus and coronary heart disease. The key targets for molecular and cellular therapy of oxidative stress in diseases of atherosclerotic genesis can be, firstly, receptors localized on the cell membrane, the binding of which to the end products of glycolysis and proinflammatory interleukins leads to the activation of inflammatory cascades; secondly, antioxidant molecules, the content of which must be maintained at an optimal level both by alimentary and local infusion. Since the processes of β-cell damage and death are in most cases mediated by the activity of the NLRP‑3 inflammasome, it is necessary to study possible ways of destabilizing this protein complex, which help prevent the maturation and secretion of interleukins‑1β and –18. Conclusion. In addition to direct treatment, careful monitoring of biochemical markers signaling the onset of a pathological process is required, a tool for which can be tests for determining the antioxidant status. In addition, it is recommended to promote a healthy lifestyle among individuals prone to diabetes mellitus 2 and cardiovascular diseases, consisting of reducing the consumption of foods rich in fats and carbohydrates (in parallel with enriching the diet with fiber-rich, vitamins and preventing oxidative stress), increasing beneficial physical activity and quitting smoking.