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. LPO and its products disrupted nitric oxide production and reduced its bioavailability, which led to the development of endothelial dysfunction and impaired microcirculatory hemodynamics. At the same time, damage of cytoplasmic membranes of internal organs (kidney, liver, and myocardium) was revealed, which was seen from reduced Na, K-ATPase activity in homogenates of these organs and increased serum activity of organ-specific (ALT, AST, and γ-glutamyl transpeptidase) and excretory (alkaline phosphatase) enzymes.

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Chronic parenteral administration of cobalt chloride (6 mg/kg) to male rats for 2 weeks or 1 month was accompanied by activation of lipid peroxidation (LPO), a decrease of superoxide dismutase activity and an increase of catalase activity. The membrane toxic action also resulted in a decrease of cortical and medullar Na+,K+-ATPase activity of kidneys, and the decrease in renal functions (glomerular filtration, renal water reabsorption, spontaneous diuresis, electrolyte excretion).

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The study was conducted on a model of endothelial dysfunction caused by intoxication with nickel chloride and an eNOS inhibitor -L-NAME. The results showed a significant increase in oxidants and their inhibitory effect on the development of nitric oxide (NO) -a biochemical marker of the endothelial dysfunction. When introducing nickel and modified L-arginine, the internal molecular structure of endothelial NO synthase (eNOS) and the ability of the enzyme to produce nitric oxide and active oxygen metabolites (AMA) is violated. L-arginine stimulates the expression of eNOS, the development of nitric oxide and inhibits lipoperoxidation. This experimental method is relevant, because only fundamental knowledge about the mechanisms of development of endothelial dysfunction will allow us to develop a predictive approach for the prevention of negative effects.