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吲哚 - 3 - 甲醇对苯并[a]芘代谢产物与小鼠肝脏DNA和蛋白质共价结合的保护作用。

Protection by indole-3-carbinol against covalent binding of benzo[a]pyrene metabolites to mouse liver DNA and protein.

作者信息

Shertzer H G

出版信息

Food Chem Toxicol. 1983 Feb;21(1):31-5. doi: 10.1016/0278-6915(83)90265-x.

DOI:10.1016/0278-6915(83)90265-x
PMID:6298084
Abstract

Indole-3-carbinol (I-3-C) is a compound present in many cruciferous vegetables that has been shown to reduce aryl hydrocarbon-induced neoplasia in experimental animals. We examined the relationship between the ability of I-3-C to alter the activity of hepatic aryl hydrocarbon hydroxylase (AHH), and its ability to inhibit the covalent binding of benzo[a]pyrene (BaP) metabolites to DNA and protein. Using an in vitro system and a hepatic postmitochondrial fraction from mice that had been treated by gavage with I-3-C, we found that up to 90% of the covalent binding of BaP metabolites to macromolecules was eliminated, while AHH activity was unchanged. In experiments in vivo, treatment of mice by gavage with I-3-C before [14C]BaP resulted in up to an 80% decrease in covalent binding of 14C to DNA or protein with no concomitant decrease in hepatic AHH activity. These results suggest that I-3-C administered in vivo confers protection against the binding of BaP oxidation products to hepatic cellular macromolecules.

摘要

吲哚 - 3 - 甲醇(I - 3 - C)是一种存在于多种十字花科蔬菜中的化合物,已证明其能在实验动物中减少芳烃诱导的肿瘤形成。我们研究了I - 3 - C改变肝脏芳烃羟化酶(AHH)活性的能力与其抑制苯并[a]芘(BaP)代谢产物与DNA和蛋白质共价结合能力之间的关系。使用体外系统和经灌胃给予I - 3 - C处理的小鼠肝脏线粒体后组分,我们发现BaP代谢产物与大分子的共价结合消除了高达90%,而AHH活性未改变。在体内实验中,在给予[14C]BaP之前给小鼠灌胃I - 3 - C,导致14C与DNA或蛋白质的共价结合减少高达80%,而肝脏AHH活性并未随之降低。这些结果表明,体内给予I - 3 - C可对BaP氧化产物与肝脏细胞大分子的结合起到保护作用。

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