Effect of Vitamin E on alcohol-induced changes in oxidative stress and expression of transcription factors NFkB and AP-1 in mice brain cerebral hemispheres

Abstract

Redox sensitive transcription factors nuclear factor ĸB (NF-ĸB) and activator protein-1 are involved in the pathogenesis of alcohol-induced disorders. Because of its antioxidative properties, vitamin E may help prevent oxidative stress-induced disorders. The aim of the present study was to delineate the molecular mechanisms associated with alcohol-induced oxidative stress and to see whether vitamin E supplementation counters the alcohol-induced adverse effects. The results showed that vitamin E supplementation restored the redox status and thus prevented the alcohol-induced oxidative stress. Further measurements of the mRNA expressions of cjun, cfos, p65 (NFkB) indicated an increase in their expression during oxidative stress. Although Vit E inhibited NFkB activation, it stimulated AP1 expression. The results support the findings that alcohol induces oxidative stress in nervous tissue. The data further show that vitamin E can mitigate the toxic effects of alcohol and thus can be suitable as a potential therapeutic agent for alcohol-induced oxidative damage in brain.<b></b>