The antioxidative property of green tea against Iron-induced oxidative stress in rat brain

Anya M. Y. Lin ； B. Y. Chyi ； L. Y. Wu ； L. S. Hwang ； L. T. Ho

《The Chinese Journal of Physiology》 41卷4期 (1998/12) Pp. 189-194

並列摘要

The antioxidative property of green tea against iron-induced oxidative stress was investigated inthe rat brain both in vivo and in vivo.Incubation of brain homogenates at 37℃ for 4 hours in vitroincreased the formation of Schiff base fluorescent products of malonaldehyde,an indicator of lipidperoxidation.Auto-oxidation(without exogenous iron)of brain homogenates was inhibited by green teaextract in a concentration-dependent manner.Moreover,incubation with iron(1μM)elevated lipidperoxidation of brain homogenates after 4-hour incubation at 37℃.Co-incubation with green teaextract dose-dependently inhibited the iron-induced elevation in lipid peroxidation.For the in vivostudies:ferrous citrate(iron,4.2nmoles)was infused intranigrally and induced degeneration of thenigrostriatal dopaminergic system of rat brain.An increase in lipid peroxidation in substantia nigra aswell as a decrease in dopamine content in striatum was observed seven days after the iron infusion.Intranigral infusion of green tea extract alone did not increase,and in some cases,even decreased lipidperoxidation in substantia nigra.Co-infusion of green tea extract prevented oxidative injury inducedby iron.Both iron-induced elevation in lipid peroxidation in substantia nigra and iron-induced decreasein dopamine content in striatum were suppressed.Oral administration of green tea extract for two weeksdid not prevent the iron-induced oxidative injury in nigrostriatal dopaminergic system.Our resultssuggest that intranigral infusion of green tea extract appears to be nontoxic to the nigrostriataldopaminergic system.Furthermore,the potent antioxidative action of green tea extract protects thenigrostriatal dopaminergic system from the iron-induced oxidative injury.

並列關鍵字

green tea ； iron ； oxidative stress ； antioxidant ； nigrostriatal system ； lipid peroxidation