Mechanisms of endothelium and internal organs dysfunction associated with exposure to cobalt chloride (experimental study)

Cobalt administration in the human body is a risk factor for developing pulmonary and cardiovascular health problems. In this paper we report the results of functional studies and biochemical mechanisms of endothelial dysfunction and pathology of internal organs in cobalt intoxication in experiment. System-organ nature of the activation of oxidative processes is identified according to the increase of MDA secondary product in erythrocytes and homogenates of internal organs as well as the participation of AOC imbalance in the development of lipid peroxidation, the peculiarities of the violations of NO release endothelial function and participation in this process of L-arginine and an analogue of endogenous inhibitor of expression eNOS -L-NC - arginine methyl ester (L-NAME or L-nitro-arginine-methil-ester) with cobalt intoxication in conditions of activation of oxidative processes. Chronic cobalt intoxication in rats leads to the activation of oxidative processes, thus there is inhibition of superoxide dismutase activity and the concentration of catalase and ceruloplasmin increased. Cholesterol metabolism is disturbed, as well as impaired nitric oxide production and its bioavailability, which is accompanied by the change of the microcirculatory hemodynamics of the visceral organs. The evaluation of the internal organs' functional state according to the activity of the Na+,K+-ATPase in homogenates is performed, as well as due to the activity of organ-specific and excretory enzymes in blood serum on the background of cobalt toxicity. The role of changes of cholesterol metabolism is established - as a risk factor of atherogenesis in violation of the bioavailability of nitric oxide. For the pathogenetic correction of violations we applied the method using the endogenous antioxidant coenzyme Q10 and regulators of the expression eNOS L-arginine, L-NAME and their combination with coenzyme Q10.