艾氏剂、狄氏剂和毒杀芬对间隙连接介导的细胞间通讯的体外抑制:其促肿瘤和神经毒性作用的可能细胞机制。

Molecular toxicology Pub Date : 1987-01-01
J E Trosko, C Jone, C C Chang
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引用次数: 0

摘要

有毒化学物质的多效性有几种机制可以解释。虽然化学物质的细胞毒性和致突变性已经得到了很好的研究,而且相对容易检测到,但化学物质毒性的非细胞毒性和非致突变性(即表观遗传)机制还不太清楚。利用中国仓鼠细胞共培养测定V79 6-硫鸟嘌呤敏感细胞(6tg)和耐药细胞(6TGr)之间代谢合作的体外实验,已经开发出一种非细胞毒性和非致突变的化学物质,可以定量地抑制间隙连接通讯。已知对动物具有多效毒性作用的杀虫剂艾氏剂、狄氏剂和毒杀芬被证明可抑制间隙连接通讯。对结果的解释表明,对间隙连接通讯的化学抑制可能是解释其促肿瘤和神经毒性作用的可能机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inhibition of gap junctional-mediated intercellular communication in vitro by aldrin, dieldrin, and toxaphene: a possible cellular mechanism for their tumor-promoting and neurotoxic effects.

Several mechanisms have been postulated to be responsible for the pleiotropic effects of toxic chemicals. Although the cytotoxicity and mutagenicity of chemicals are well studied and relatively easily detected, the noncytotoxic and nonmutagenic (i.e., epigenetic) mechanisms of chemical toxicity are less well understood. An in vitro assay, using cocultures of Chinese hamster cells to measure metabolic cooperation between V79 6-thioguanine-sensitive (6TGs) and resistant (6TGr) cells, has been developed to detect noncytotoxic and nonmutagenic chemicals that inhibit, quantitatively, gap junctional communication. The insecticides aldrin, dieldrin, and toxaphene, known to have pleiotropic toxic effects in animals, were shown to inhibit gap junctional communication. Interpretation of results suggests that chemical inhibition of gap junctional communication could be a possible mechanism to explain their tumor-promoting and neurotoxic effects.

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