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谷胱甘肽过氧化物酶活性下降是脑衰老的一个原因:食用绿茶儿茶素可防止衰老小鼠大脑中其活性下降和蛋白质氧化损伤。

Decline in glutathione peroxidase activity is a reason for brain senescence: consumption of green tea catechin prevents the decline in its activity and protein oxidative damage in ageing mouse brain.

作者信息

Kishido Takahiro, Unno Keiko, Yoshida Hirotoshi, Choba Daisuke, Fukutomi Rie, Asahina Shunsuke, Iguchi Kazuaki, Oku Naoto, Hoshino Minoru

机构信息

Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka, 422-8526, Japan.

出版信息

Biogerontology. 2007 Aug;8(4):423-30. doi: 10.1007/s10522-007-9085-7. Epub 2007 Feb 20.

DOI:10.1007/s10522-007-9085-7
PMID:17310319
Abstract

The accumulation of oxidative damage is believed to contribute to senescence. We have previously found that the consumption of green tea catechins (GT-catechin), which are potent antioxidants, decreases oxidative damage to DNA and improves brain function in aged mice with accelerated senescence (SAMP10 mice). To investigate the mechanisms underlying the beneficial effects of GT-catechin, we measured the activities of antioxidative enzymes in the brains of aged SAMP10 mice. The activity of glutathione peroxidase (GPx), an essential enzyme for reduction of hydrogen and lipid peroxides, was significantly lower in aged mice than in younger ones. However, the decline in activity was prevented in aged mice that had consumed GT-catechin. The increased level of carbonyl proteins, a marker of oxidative damage in proteins, was also significantly reduced in aged mice that had consumed GT-catechin. The activities of superoxide dismutase and catalase were not decreased in aged mice. These results suggest that decreased activity of GPx importantly contributes to brain dysfunction in ageing SAMP10 mice. Furthermore, the intake of GT-catechin protected the decline in GPx activity and age-related oxidative damage in the brain.

摘要

氧化损伤的积累被认为与衰老有关。我们之前发现,食用绿茶儿茶素(GT-儿茶素),一种强大的抗氧化剂,可减少对DNA的氧化损伤,并改善加速衰老的老年小鼠(SAMP10小鼠)的脑功能。为了研究GT-儿茶素有益作用的潜在机制,我们测量了老年SAMP10小鼠大脑中抗氧化酶的活性。谷胱甘肽过氧化物酶(GPx)是还原氢和脂质过氧化物的必需酶,其活性在老年小鼠中显著低于年轻小鼠。然而,食用GT-儿茶素的老年小鼠的活性下降得到了预防。蛋白质氧化损伤的标志物羰基蛋白水平的升高,在食用GT-儿茶素的老年小鼠中也显著降低。超氧化物歧化酶和过氧化氢酶的活性在老年小鼠中没有降低。这些结果表明,GPx活性降低是导致衰老SAMP10小鼠脑功能障碍的重要原因。此外,摄入GT-儿茶素可保护大脑中GPx活性的下降和与年龄相关的氧化损伤。

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