Dynamics of superoxide dismutase-1 gene expression in different types of drug correction of toxic disorders in the liver

Abstract

Introduction. Drugs are needed to counteract oxidative stress to prevent toxic liver damage. Relevant and promising is the use of analysis of changes in gene expression under the influence of drugs to assess the effectiveness of their use and identify the molecular genetic mechanisms of the development of hepatotoxicity. The purpose of this study was to examine the effect of the drugs “Heptor”, “Mexidol”, and “Oxymethyluracil” (OMU) on the level of expression of the Sod1 gene in the liver of rats with carbon tetrachloride lesion of the liver. Material and methods. The experiment was performed on 70 male outbred white rats. The control group received olive oil subcutaneously; first experimental group - subcutaneous carbon tetrachloride (CTC); second experimental group - CTC and intraperitoneal “Heptor”; third experimental - CTC and subcutaneous “Mexidol”; fourth experimental - CTC and oral OMU. The material was collected at two-time intervals, 24 and 72 hours. To analyze the expression of the studied gene, quantitative RT-PCR in real-time mode was carried. Results. The use of all three drugs after 72 h resulted in a decrease in the Sod1 gene expression level under oxidative stress induced by CTC. OMU exerted the most significant influence on the transcriptional activity of the Sod1 gene. Limitations. The limitations of the study are due to the methodology of the analysis: since expression was evaluated by quantitative RT-PCR in real time, we evaluated the transcriptional activity of the gene without taking into account further post-transcriptional regulation of expression. Conclusion. The study results indicate the ability of the studied hepatoprotectors to suppress the expression of the Sod1 gene in rat liver when exposed to CTC. It can be assumed that the studied drugs, through a change in the expression of the Sod1 gene, can participate in the regulation of free radical processes in liver damage.