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白茶对F344大鼠中2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶诱导的结肠异常隐窝的抑制作用。

Inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced colonic aberrant crypts in the F344 rat.

作者信息

Santana-Rios G, Orner G A, Xu M, Izquierdo-Pulido M, Dashwood R H

机构信息

Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.

出版信息

Nutr Cancer. 2001;41(1-2):98-103. doi: 10.1080/01635581.2001.9680618.

DOI:10.1080/01635581.2001.9680618
PMID:12094635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2367318/
Abstract

There is growing interest in the potential health benefits of tea, including the anticarcinogenic properties. We report here that white tea, the least processed form of tea, is a potent inhibitor of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced colonic aberrant crypts in the rat. Male Fischer 344 rats were treated for 8 wk with white tea (2% wt/vol) or drinking water alone, and on alternating days in experimental Weeks 3 and 4 the animals were given PhIP (150 mg/kg body wt p.o.) or vehicle alone. At the end of the study there were 5.65 +/- 0.81 and 1.31 +/- 0.27 (SD) aberrant crypt foci per colon in groups given PhIP and PhIP + white tea, respectively (n = 12, P < 0.05). No changes were detected in N-acetyltransferase or arylsulfotransferase activities compared with controls, but there was marked induction of ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, and UDP-glucuronosyltransferase after treatment with white tea. Western blot revealed corresponding increases in cytochrome P-450 1A1 and 1A2 proteins. Enzyme assays and Western blot also revealed induction of glutathione S-transferase by white tea. There was less parent compound and 4'-hydroxy-PhIP but more PhIP-4'-O-glucuronide and PhIP-4'-O-sulfate in the urine from rats given PhIP + white tea than in urine from animals given carcinogen + drinking water. The results indicate that white tea inhibits PhIP-induced aberrant crypt foci by altering the expression of carcinogen-metabolizing enzymes, such that there is increased ring hydroxylation at the 4' position coupled with enhanced phase 2 conjugation.

摘要

茶对健康的潜在益处,包括抗癌特性,正受到越来越多的关注。我们在此报告,白茶作为加工最少的茶类,是大鼠中2-氨基-1-甲基-6-苯基咪唑[4,5-b]吡啶(PhIP)诱导的结肠异常隐窝的有效抑制剂。雄性Fischer 344大鼠用白茶(2%重量/体积)或仅饮用水处理8周,在实验第3周和第4周隔天给动物口服PhIP(150毫克/千克体重)或仅给予赋形剂。研究结束时,给予PhIP组和PhIP +白茶组的每结肠异常隐窝病灶分别为5.65±0.81和1.31±0.27(标准差)(n = 12,P < 0.05)。与对照组相比,未检测到N-乙酰转移酶或芳基磺基转移酶活性的变化,但白茶处理后乙氧基异吩唑酮O-脱乙基酶、甲氧基异吩唑酮O-脱甲基酶和UDP-葡萄糖醛酸基转移酶有明显诱导。蛋白质印迹显示细胞色素P-450 1A1和1A2蛋白相应增加。酶分析和蛋白质印迹还显示白茶诱导了谷胱甘肽S-转移酶。给予PhIP +白茶的大鼠尿液中母体化合物和4'-羟基-PhIP较少,但PhIP-4'-O-葡萄糖醛酸苷和PhIP-4'-O-硫酸盐比给予致癌物+饮用水的动物尿液中更多。结果表明,白茶通过改变致癌物代谢酶的表达来抑制PhIP诱导的异常隐窝病灶,从而使4'位的环羟基化增加并伴有第二相结合增强。

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