Joint Effects of Mexidol and Nitroglycerine on Nitric Oxide Formation in Animal Liver Tissues

Taasilkan Zhumabaeva,Nurbek Bopoev,Zoya Kuropteva,Nazgul Zhumabaeva,Amanai Kadyrbaeva,Zhoomart Moldaliev,Zhypargul Abdullaeva

doi:10.4236/ajmb.2021.113007

Abstract

This work is investigating Mexidol (2-ethyl-6-methyl-3-hydroxy pyridine succinate) effect on the formation of nitric oxide (NO) in animal liver tissues, which is a regulator of many physiological processes and plays an important role in the vascular relaxation, neurotransmission and immune system functioning. Analyses performed by EPR spectroscopy revealed Hem-NO complex signals from paramagnetic centers in arbitrary units; produced nitrogen oxide amount in liver tissues was determined by method of double integration signals from nitrosyl complexes.

Highlights

Analyses performed by EPR spectroscopy revealed Hem-nitric oxide (NO) complex signals from paramagnetic centers in arbitrary units; produced nitrogen oxide amount in liver tissues was determined by method of double integration signals from nitrosyl complexes
The nature of mexidol and nitroglycerine joint effects on the nitric oxide formation in the liver tissue was unknown until the relaxation factor stimulating the formation of cyclic guanosine monophosphate, which serves as a secondary mediator for neurotransmitters and hormones that can influence guanylate cyclase and have a vasodilation effect had been found
Analysis of the EPR spectra obtained from liver tissue samples incubated only with Mexidol for 24 h at room temperature and control samples incubated under the same conditions showed, that NO is formed in liver tissue samples after incubation with Mexidol (Figure 1)

Summary

Introduction

Pretreatment with mexidol under conditions of acute liver damage in rats showed inhibition of lipid peroxidation, normalization of enzymes-markers activity in damage of hepatocytes, and normalization of blood serum bilirubin level; mexidol (3-hydroxy-6-methyl-2-ethylpyridine succinate) influences the state of homeostasis in guinea pigs intoxicated with paracetamol [1] [2]. When activated by bacterial endotoxins or T-lymphocytes, macrophages activate the synthesis of iNOS enzyme, participating in a pathway converting arginine to nitric oxide. There, nitric oxide inhibits vital groups of enzymes: the mitochondrial respiratory chain of the Krebs cycle and DNA synthesis. Under these conditions, energy production and cell division become impossible which can lead to cell death. To understand the nature of cytostatic and cytotoxic signals, it is necessary to consider reactions with oxygen and superoxide radicals The products of these reactions are peroxynitrites and are responsible for the toxic effects of nitrogen oxide (NO). Suppression of aconitase in the Krebs cycle [14], ribonucleotide reductase, interaction with thiols, and depletion of energy reserves currently discussed as possible pathways for cell death

In Vitro Experiments on Liver Tissue

EPR Spectra

Hem-NO and EPR Reference Signals

Results and Discussions

Conclusion