[Expression of Cell Cycle, Oxidative Stress, and Apoptosis Related Genes Chek1, Hmox1, Casp7 in Rat Liver Exposed to Carbon Tetrachloride].

Carbon tetrachloride is a well-studied hepatotropic poison. Animal models of exposure to carbon tetrachloride resemble acute liver damage in humans. This paper presents the study of the expression of genes related to cell cycle control, apoptosis, and oxidative stress in a model of carbon tetrachloride-induced toxic hepatitis in rats. White mongrel male rats were injected with a 50% oil solution of carbon tetrachloride at a dose of 0.125-4.000 g/kg (experimental group) or olive oil (control group). The animals were decapitated 24 and 72 h after the administration of carbon tetrachloride, and the qRT-PCR expression levels of the genes encoding hemoxygenase-1 (Hmox1), cell cycle checkpoint kinase-1 (Chek1), and caspase-7 (Casp7) in the liver were analyzed. The increase in the expression levels of Hmox1 and Chek1 after exposure was detected. These genes may either play a role in promoting pathological oxidative stress in the liver or be a part of a stress response. We have concluded that the major pathway of the liver damage in carbon tetrachloride exposed animals is necrosis rather than apoptosis.

[GENETIC PREDISPOSITION TO DEVELOPMENT OF TOXIC HEPATITIS].

Aim: The aim of this study was to investigate the frequency of polymorphic variants of genes CYP2E1 and GSTA1 in patients with pathology of the hepatobiliary system (PHS) and healthy individuals in the Republic of Bashkortostan, as well as an analysis of possible associations of genotypes of this gene with the development of PHS. Materials and methods: There were examined 81 patients with pathology of the hepatobiliary system. Was studied association analysis of polymorphic loci of genes CYP2E1 and GSTA1. Results: The study demonstrated that a marker of risk of developing the disease is AA genotype (OR = 2,09; 95% CI 1,07-4,10) polymorphic locus gene rs3957357 GSTA1.