Oxidative stress in mitochondria of the brain tissue with aluminum neurotoxycosis and applying of glutathione and modulators of coenzyme A biosynthesis

Abstract

Using an experimental model of aluminum neurotoxicosis, it was established that under conditions of chronic administration of aluminum chloride to rats, oxidative stress develops and inhibits the redox potential of the glutathione system in the mitochondrial and postmitochondrial fractions of the cerebral hemispheres. It was shown that the ingestion of N-acetylcysteine, as well as its combined use with coenzyme A biosynthesis precursors (D-panthenol or D-pantetin) against the background of aluminum neurotoxicosis, leads to a marked decrease in the production of reactive oxygen species by mitochondria, a decrease in the production of thiobarbituric acid reactive substances, and normalization of GSH content and its biosynthesis in brain tissue. The results indicate a high efficiency of the biosynthesis precursor of glutathione N-acetylcysteine in the prevention of oxidative stress in the chronic model of aluminum neurotoxicosis, which may be the rationale for its use as a modulator of mitochondrial redox status in the development of neurodegenerative pathology.