Metabolic and functional disorders in rats with cadmium intoxication and their pathogenetic correction

Introduction. The relevance of the study is due to the high prevalence of diseases caused by exposure to harmful substances, such as cadmium, which is an environmental and professional hazard. Modeling the intoxication syndrome in animals and developing strategies for its correction allow us to identify effective methods of prevention and therapy, which is especially important for combating toxic effects and preventing the development of severe pathologies of the liver, kidneys and cardiovascular system. Aim: To study influence of cadmium sulfate on the changes in metabolic and functional parameters of blood and organs and their pathogenetic correction. Material and Methods. The intoxication syndrome was modeled on 65 rats, by exposure to cadmium sulfate in an amount of 1 mg/ kg of body weight intramuscularly. After creating systematic daily intoxication lasting 30 days, L-arginine (10 mg/kg of animal body weight) was injected intramuscularly and kudesan (10 mg/kg) orally. Results. The applied drugs had an inhibitory effect on the activity of oxidative stress, decreased the level of malonate dialdehyde in the blood and in the cortex and medulla of the renal tissue, compared with the results indicating cadmium intoxication. The severity of lipid peroxidation was also reduced in the liver parenchyma. At the same time, positive dynamics of the antioxidant system activity and an increase in the activity of SOD, as well as total metabolites of nitric oxide – NOx were revealed. The use of corrective drugs – L-arginine and kudesan provided a lower level of LDL-C with an increase in HDL-C. From the side of the main processes of urine formation, an increase in SCF, water and sodium transport in the renal tubules was shown due to a higher activity of Na, K-ATPase in the cortex and medulla of the kidneys. A negative correlation was found between the decrease in MDA content, the increase in NOx concentration and the activation of Na, K-ATPase (r = –0.67, p < 0.05; r = –0.69, p < 0.05). A decrease in the activity level of organspecific enzymes in blood plasma indicates an improvement in liver function. Conclusion. Cadmium intoxication is characterized by the development of oxidative stress, decreased NOx levels as a major vasodilator, and increased atherogenic lipoprotein levels in the blood plasma. These biochemical changes disrupt microcirculatory hemodynamics and the functional capacity of renal and hepatic tissue. Corrective therapy with the medicinal agents L-arginine and kudesan for cadmium intoxication effectively suppressed oxidative stress and improved cholesterol and nitric oxide metabolism. The combination of these metabolic parameters in the intoxication syndrome was accompanied by increased renal and hepatic function, improved parameters of key urine formation processes, and decreased levels of organ-specific enzymes in the blood plasma. This approach to pathogenetic correction opens up prospects for clinical application in toxicology and preventive medicine.