Analysis of Mechanisms Underlying the Development of Endothelial Dysfunction and Functional Disorders in Experimental Diabetes Mellitus and Their Pathogenetic Correction.

On the model of alloxan-induced diabetes mellitus in rats, the development of oxidative stress and violation of the NO-producing function of the endothelium and internal organs was established. Structural changes in the vascular endothelium due to increased level of atherogenic LDL preventing access of L-arginine to endothelial NO synthase (eNOS) contribute to the development of endothelial dysfunction, which is paralleled by oxidative modification of L-arginine and the formation of inhibitors of eNOS expression (asymmetric dimethylarginine, L-NAME). These findings are indicative of reduced eNOS expression in experimental diabetes mellitus.

Analysis of the Mechanisms of Impairment of Functional Parameters of Internal Organs in Saturnism in an Experiment in Rats.

In rats with lead intoxication (intramuscular administration of lead acetate in a dose 5 mg/kg for 30 days), the development of oxidative stress, reduced expression of endothelial NO synthase and total metabolites of NO production, as well as an increased content of norepinephrine were observed. Lead-induced nephropathy developed; diuresis and sodium excretion increased due to a decrease in tubular transport of water and sodium ions. Activation of free-radical reactions in cells of the renal cortex and medulla contributed to inhibition of Na,K-ATPase.

Oxidative Stress and Biochemical Markers of Endothelial Dysfunction and Organ Damage under Conditions of Experimental Nonferrous Metal Intoxication.

Chronic nickel intoxication caused by parenteral nickel chloride administration (0.5 mg/kg of body weight) to Wistar rats led to ROS generation inducing LPO in erythrocyte membranes and homogenates of renal, liver, and myocardial tissue. Superoxide dismutase (SOD) activity was inhibited, while catalase activity and ceruloplasmin concentration increased.

[MECHANISMS OF AFOBAZOLE INFLUENCE ON THE NO PRODUCING ENDOTHELIUM FUNCTION AND INDICATORS OF OXIDATIVE STRESS IN RATS WITH EXPERIMENTAL DIABETES MELLITUS.].

Data on the mechanisms of afobazole effect on the NO-producing function of endothelium under conditions of oxidative stress in rats with experimental diabetes mellitus are presents. It is established for the first time that the drug in vivo inhibits the intensity of lipid peroxidation, reduces the concentration of malonic dialdehyde in red blood cells up to 16.07% (p = 0.

[Effect of L-carnitine, afobazole and their combination with L-arginine on biochemical and histological indices of endothelial disfunction in cobalt intoxication in rats].

The influence of L-carnitine and afobazole and their combination with L-arginine on biochemical and histological indices of endothelial dysfunction in rats with cobalt intoxication. The obtained data revealed biochemical markers of endothelial dysfunction. Found that-in rats with cobalt intoxication during treatment occurred inhibition of lipid peroxidation (LPO), reduced the concentration of malondialdehyde (MDA) in erythrocytes, activation of superoxide dismutase (SOD).