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.
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Authors | Jasmeet Kaur, M P Bansal |
Journal | Indian journal of experimental biology
(Indian J Exp Biol)
Vol. 46
Issue 8
Pg. 562-7
(Aug 2008)
ISSN: 0019-5189 [Print] India |
PMID | 18814483
(Publication Type: Journal Article)
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Chemical References |
- NF-kappa B
- RNA, Messenger
- Transcription Factor AP-1
- Vitamin E
- Ethanol
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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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