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

Abstract
Redox sensitive transcription factors nuclear factor kappaB (NF-kappaB) 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 (NFkappaB) indicated an increase in their expression during oxidative stress. Although Vit E inhibited NFkappaB 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.
AuthorsJasmeet Kaur, M P Bansal
JournalIndian journal of experimental biology (Indian J Exp Biol) Vol. 46 Issue 8 Pg. 562-7 (Aug 2008) ISSN: 0019-5189 [Print] India
PMID18814483 (Publication Type: Journal Article)
Chemical References
  • NF-kappa B
  • RNA, Messenger
  • Transcription Factor AP-1
  • Vitamin E
  • Ethanol
Topics
  • Animals
  • Brain (drug effects, metabolism)
  • Ethanol (pharmacology)
  • Gene Expression Regulation (drug effects)
  • Male
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B (genetics)
  • Oxidative Stress (drug effects)
  • RNA, Messenger (genetics)
  • Transcription Factor AP-1 (genetics)
  • Vitamin E (pharmacology)

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