Vitamin E restores amyloid peptide (25-35) induced changes in cellular redox in C6 glioma cells; Implications to Alzheimers disease

被引:0
作者
Ayasolla, K
Singh, AK
Singh, I
机构
来源
XI BIENNIAL MEETING OF THE SOCIETY FOR FREE RADICAL RESEARCH INTERNATIONAL | 2002年
关键词
Alzheimer's Disease(AD); iNOS; oxidative stress; vitamin E; MnSOD; and ROS (reactive oxygen species);
D O I
暂无
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
betaeta amyloid peptide accumulation and its deposition in certain areas of the brain as plaques appears to play a significant role in beta amyloid induced toxicity in Alzheimer's disease (AD). Amyloid peptides (1-42, 1-40 and 25-35) have been demonstrated to induce increased ROS (Reactive oxygen species) production, leading to severe oxidative stress conditions in several different cell lines. Here we present evidence that soluble beta amyloid peptide (25-35) and cytokine (LPS, IFN-gamma) alter the cellular redox, thus leading to the induction of antioxidant enzymes namely the Manganese Superoxide dismutase (MnSOD) and Copper Zinc Superoxide dismutase (Cu/ZnSOD), reduction in the levels of glutathione and a concomitant increase in the induction of iNOS (inducible nitric oxide synthase) and production of Nitric oxide (NO). Vitamin E treatment blocked the betaA/cytokine induced reduction of glutathione and induction of MnSOD, Cu/ZnSOD and iNOS. The near normalization of levels of glutathione and attenuation of the induction of antioxidant enzymes and iNOS and thereby the cellular redox by Vitamin E in cytokine -betaA(25-35) treated cells suggests a relationship between cellular redox and the inflammatory disease process.
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页码:503 / 508
页数:6
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