The Influence of the Antioxidant System on Endothelial Dysfunction in Patients with Diabetic Nephropathy
Goyushova R. R

The blood parameters was investigated in 46 patients with conservative stage of chronic renal failure. The development of endothelial dysfunction was observed with worsening of renal failure from diabetes. We identified a relationship between the acceleration of lipid peroxidation and decreased levels of nitric oxide in the peripheral blood in the development of endothelial dysfunction in diabetic nephropathy. Reactive oxygen species (ROS) play a significant role in the pathogenesis of many chronic diseases, such as diabetes and chronic renal insufficiency (1, 2,). In addition to lipid peroxidation, in recent years, researchers have focused on studying endothelial function in normal and various pathological processes(3, 4). According to the literature, the leading causes of endothelial dysfunction include decreased availability of nitric oxide (NO), reduced levels of tetrahydrobiopterin (BH4) and glutathione (GSH), oxidative stress and the accumulation of peroxides (5,6). In patients with diabetes mellitus, early impaired endothelium-dependent vasodilatation is also present (7). In diabetic nephropathy, nitric oxide (NO) synthesis is impaired in endothelial cells. NO exhibits powerful vasodilator, antiplatelet, anti-proliferative and anti-atherogenic activities. The neutralization of this molecule leads to increased blood pressure, the development of thrombosis and progression to atherosclerosis (8). It was revealed the information about significant impairment of endothelium-dependent vasodilation and oxidative stress, and some even reacquire intact kidney filtration dysfunction in diabetic patients. In the pathological process of chronic renal failure, which develops in diabetic patients and is even more exacerbated, the degree of extracellular and intracellular oxidative stress correlates with the severity of renal failure (8, 9). In similar pathologies, the early inactivation of NO is due to the glycosylation of end products and oxidizing radicals resulting from chronic hyperglycemia (10, 11). Despite numerous studies on the process of lipid peroxidation and antioxidant components in diabetic nephropathy, the role of lipid peroxidation in the development of endothelial dysfunction is not fully understood. The aim of the present investigation was to study the endothelial dysfunction associated with antioxidant system (AOS) injury in patients with diabetic nephropathy.

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