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多氯联苯、多氯二苯并 - 对 - 二噁英和多氯二苯并呋喃在实验动物中的生物学效应机制

Mechanisms of the biological effects of PCBs, polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans in experimental animals.

作者信息

Neal R A

出版信息

Environ Health Perspect. 1985 May;60:41-6. doi: 10.1289/ehp.856041.

DOI:10.1289/ehp.856041
PMID:2992926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1568561/
Abstract

Polychlorinated biphenyls, certain polychlorinated dibenzo-p-dioxins and certain polychlorinated dibenzofurans cause a variety of biological effects in experimental animals. The mechanism of the induction of certain enzymes is perhaps best understood. That is, there is binding of certain chlorinated biphenyls, dibenzo-p-dioxins and dibenzofurans to a receptor, translocation of the compound-receptor complex into the nucleus followed by an increased activity of a number of enzymes in the cell. Although the concentration of this receptor in various tissues of some mouse strains correlates well with the intensity of some of the biological effects observed in the mouse strains exposed to these compounds, this correlation apparently does not extend across various species. The current evidence suggests that the acute toxic effects of TCDD in various species is in some way associated with binding of TCDD to the receptor. However, biological effects of TCDD in addition to those resulting from binding to the receptor may be required to produce acute toxicity and, perhaps, other effects. The acute toxic effects of TCDD are probably caused by the parent compound rather than metabolites; however, this conclusion must be viewed as tentative. Also, it cannot be excluded at this time that biological effects other than acute toxicity may be caused by metabolites of TCDD. Finally, the acute toxic effects of TCDD appear not to be related, at least not directly, to the rate of metabolism of TCDD in experimental animals nor to the half-life of excretion.

摘要

多氯联苯、某些多氯二苯并 - 对 - 二噁英和某些多氯二苯并呋喃在实验动物中会引发多种生物学效应。对某些酶诱导机制的理解或许最为透彻。也就是说,某些氯化联苯、二苯并 - 对 - 二噁英和二苯并呋喃会与一种受体结合,化合物 - 受体复合物转位进入细胞核,随后细胞内多种酶的活性增加。尽管在某些小鼠品系的各种组织中这种受体的浓度与在接触这些化合物的小鼠品系中观察到的某些生物学效应的强度密切相关,但这种相关性显然并不适用于所有物种。目前的证据表明,TCDD在各种物种中的急性毒性效应在某种程度上与TCDD与受体的结合有关。然而,除了与受体结合所产生的效应之外,TCDD的生物学效应可能还需要产生急性毒性以及或许其他效应。TCDD的急性毒性效应可能是由母体化合物而非代谢产物引起的;然而,这一结论必须视为初步的。此外,目前不能排除TCDD的代谢产物可能会引起除急性毒性之外的其他生物学效应。最后,TCDD的急性毒性效应似乎与实验动物中TCDD的代谢速率以及排泄半衰期至少没有直接关系。

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