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咖啡因和黄烷醇在绿茶诱导肝脏Ⅱ相活性中的作用。

Contribution of caffeine and flavanols in the induction of hepatic Phase II activities by green tea.

作者信息

Bu-Abbas A, Clifford M N, Walker R, Ioannides C

机构信息

School of Biological Sciences, University of Surrey, Guildford, UK.

出版信息

Food Chem Toxicol. 1998 Aug;36(8):617-21. doi: 10.1016/s0278-6915(98)00019-2.

Abstract

Aqueous extracts of green tea, at concentrations of 2.5. 5.0 and 7.5%, were administered to rats as the sole drinking fluid for 4 weeks. Hepatic glutathione S-transferase (GST) activity, determined using 1-chloro-2,4-dinitrobenzene (CDNB) and 3,4-dichloronitrobenzene (DCNB) as substrates, and UDP-glucuronosyl transferase activity, determined using 2-aminophenol as substrate, were induced but the effect was not always dose dependent. At the two highest doses, hepatic catalase activity was inhibited. In a second study, animals were exposed for 4 weeks to aqueous extracts (2.5%, v/v) of green tea, black tea (which has a much lower content of flavanols compared with green tea) and decaffeinated black tea. Treatment with the black tea enhanced GST activity, whether monitored using CDNB or DCNB, and the glucuronidation of 2-aminophenol. Treatment with decaffeinated black tea failed to modulate any of these activities, whereas treatment with green tea only enhanced the glucuronidation of 2-aminophenol. Finally, at this concentration of tea extract administration, black and decaffeinated black tea, but not green tea, suppressed catalase activity. It is concluded that neither flavanols nor caffeine are responsible for the induction of hepatic Phase II activities and inhibition of catalase activity in the rat.

摘要

将浓度为2.5%、5.0%和7.5%的绿茶水提取物作为唯一饮用水给予大鼠,持续4周。以1-氯-2,4-二硝基苯(CDNB)和3,4-二氯硝基苯(DCNB)为底物测定的肝谷胱甘肽S-转移酶(GST)活性,以及以2-氨基酚为底物测定的UDP-葡萄糖醛酸基转移酶活性均被诱导,但这种作用并不总是呈剂量依赖性。在两个最高剂量下,肝过氧化氢酶活性受到抑制。在第二项研究中,动物暴露于绿茶、红茶(与绿茶相比,黄烷醇含量低得多)和脱咖啡因红茶的水提取物(2.5%,v/v)中4周。用红茶处理可增强GST活性(无论使用CDNB还是DCNB测定)以及2-氨基酚的葡萄糖醛酸化作用。用脱咖啡因红茶处理未能调节这些活性中的任何一项,而用绿茶处理仅增强了2-氨基酚的葡萄糖醛酸化作用。最后,在这种茶提取物给药浓度下,红茶和脱咖啡因红茶,但不是绿茶,抑制了过氧化氢酶活性。得出的结论是,黄烷醇和咖啡因均与大鼠肝脏II相活性的诱导和过氧化氢酶活性的抑制无关。

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