期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：2006
卷号：38
期号：3
页码：161-166
DOI：10.3164/jcbn.38.161
出版社：The Society for Free Radical Research Japan
摘要：To determine whether lipid peroxidation induced by reactive oxygen species (ROS) is a causal factor of neurodegeneration during brain aging, we investigated whether F2-isoprostanes, non-cyclooxygenase-derived prostanoids, are formed in the rat brain and plasma by hyperoxia as oxidative stress, and whether their formation is associated with vitamin E status in vivo in association with changes that occur during brain aging. Young rats subjected to hyperoxia for 48 h revealed a marked increase in the levels of F2-isoprostanes in the brain, but not in plasma. A similar increase in F2-isoprostane level was observed in aged rats kept in normal atmosphere. Vitamin E supplementation to young rats markedly inhibited F2-isoprostane formation even after hyperoxia. In contrast, vitamin E-deficient young rats kept in normal atmosphere showed a significant increase in F2-isoprostane level in the brain. These findings indicate that F2-isoprostane formation in the brain has important implications in the etiology of neurodegenerative diseases including Alzheimer’s disease during aging, and that the analysis of F2-isoprostane level in plasma does not always reflect neuronal damage cause by oxidative stress. Vitamin E may protect neuronal damage in the brain caused by oxidative stress experienced for a long period during aging.
关键词：F2-isoprostane;Oxidative stress;Neurodegeneration;Brain;Vitamin E
