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将遗传毒性化合物解毒作为限制其致癌性的一种阈值机制。

Detoxification of genotoxic compounds as a threshold mechanism limiting their carcinogenicity.

作者信息

De Flora S

出版信息

Toxicol Pathol. 1984;12(4):337-43. doi: 10.1177/019262338401200406.

Abstract

In vitro metabolic trends were assessed for 100 genotoxic agents detected in two bacterial test systems, i.e., the Ames reversion test and a liquid DNA-repair test in Escherichia coli. Seventy-five compounds were found to undergo a more or less pronounced decrease of genotoxicity, in at least one of these models, in the presence of rat liver homogenates or in other metabolic systems (up to 40 different preparations, from various sources, for chromium compounds). A number of these deactivable compounds are reported in the literature to yield negative or equivocal results in animal carcinogenicity assays, which may imply the existence of metabolically regulated thresholds in the initiation of cancer. Several examples are provided to support this hypothesis. The in vitro treatment with a pharmacologic agent (N-acetylcysteine) enhanced detoxification mechanisms, either by stimulating enzyme activities promoting glutathione formation in liver homogenates or by reacting itself with direct-acting mutagens and with the genotoxic metabolites of procarcinogens.

摘要

对在两种细菌测试系统中检测到的100种遗传毒性剂进行了体外代谢趋势评估,这两种系统分别是艾姆斯回复突变试验和大肠杆菌中的液体DNA修复试验。在大鼠肝脏匀浆或其他代谢系统(多达40种来自不同来源的不同制剂,用于铬化合物)存在的情况下,发现75种化合物在这些模型中的至少一种中,其遗传毒性或多或少会明显降低。文献报道,许多这些可失活的化合物在动物致癌性试验中产生阴性或不确定的结果,这可能意味着癌症起始过程中存在代谢调节阈值。提供了几个例子来支持这一假设。用一种药剂(N - 乙酰半胱氨酸)进行体外处理可增强解毒机制,要么通过刺激促进肝脏匀浆中谷胱甘肽形成的酶活性,要么通过其自身与直接作用的诱变剂以及前致癌物的遗传毒性代谢物发生反应。

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