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消毒副产物的毒性相互作用研究。

Studies of the toxic interactions of disinfection by-products.

作者信息

Laurie R D, Bercz J P, Wessendarp T K, Condie L W

出版信息

Environ Health Perspect. 1986 Nov;69:203-7. doi: 10.1289/ehp.8669203.

DOI:10.1289/ehp.8669203
PMID:3816723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1474302/
Abstract

A large number and variety of compounds are formed in the process of chlorinating drinking water. The classes of compounds formed include trihalomethanes, haloacetic acids, haloacetonitriles, halophenols, and halopropanones. Many of the compounds have been shown to be toxic and are currently being further evaluated by the U.S. Environmental Protection Agency (EPA). One group of the halopropanones found in chlorinated drinking water is the dichloropropanones. The toxicological properties of this group have not been well characterized. In addition, a number of investigators have shown that ketones potentiate the hepatotoxicity of haloalkanes. We conducted a series of studies to explore both the toxicity of the dichloropropanones and their potential interactions with a well-characterized haloalkane, carbon tetrachloride. A variety of toxicological and biochemical endpoints were used to evaluate the toxicity of the dichloropropanones and their interaction with CCl4, including cytochrome P-450 concentration, reduced glutathione levels, pentane generation, serum enzyme activities, and histopathology. Administration of 1,1-dichloropropanone (DCP) resulted in elevated serum enzymes associated with periportal necrosis. Glutathione levels were reduced by the administration of 1,1-DCP; pentane generation was not increased. When 1,1-DCP was given prior to CCl4, the data were consistent with additivity. Administration of 1,3-DCP did not result in elevated serum enzymes, nor was there histopathologic evidence of necrosis. Glutathione levels and pentane generation in the 1,3-DCP-treated groups were the same as those of controls. Inhibition of the toxicologic effects of CCl4 in a dose-related manner was observed when 1,3-DCP was administered prior to CCl4.

摘要

在饮用水氯化过程中会形成大量且种类繁多的化合物。所形成的化合物类别包括三卤甲烷、卤乙酸、卤乙腈、卤酚和卤代丙酮。许多这类化合物已被证明具有毒性,美国环境保护局(EPA)目前正在对其进行进一步评估。在氯化饮用水中发现的一类卤代丙酮是二氯丙酮。该类化合物的毒理学特性尚未得到充分表征。此外,一些研究人员表明,酮类会增强卤代烷烃的肝毒性。我们进行了一系列研究,以探究二氯丙酮的毒性及其与一种特征明确的卤代烷烃四氯化碳的潜在相互作用。使用了多种毒理学和生化终点指标来评估二氯丙酮的毒性及其与四氯化碳的相互作用,包括细胞色素P - 450浓度、还原型谷胱甘肽水平、戊烷生成量、血清酶活性和组织病理学。给予1,1 - 二氯丙酮(DCP)会导致与门静脉周围坏死相关的血清酶升高。给予1,1 - DCP会降低谷胱甘肽水平;戊烷生成量未增加。当在给予四氯化碳之前给予1,1 - DCP时,数据符合相加作用。给予1,3 - 二氯丙酮不会导致血清酶升高,也没有坏死的组织病理学证据。1,3 - 二氯丙酮处理组的谷胱甘肽水平和戊烷生成量与对照组相同。当在给予四氯化碳之前给予1,3 - 二氯丙酮时,观察到其对四氯化碳毒理学效应的抑制作用呈剂量相关。

相似文献

1
Studies of the toxic interactions of disinfection by-products.消毒副产物的毒性相互作用研究。
Environ Health Perspect. 1986 Nov;69:203-7. doi: 10.1289/ehp.8669203.
2
Mechanisms of chloroform and carbon tetrachloride toxicity in primary cultured mouse hepatocytes.氯仿和四氯化碳对原代培养小鼠肝细胞毒性的作用机制
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3
Reproductive toxicology of disinfection by-products.消毒副产物的生殖毒理学
Environ Health Perspect. 1986 Nov;69:177-82. doi: 10.1289/ehp.8669177.
4
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Toxicology. 2000 Jun 8;147(2):109-31. doi: 10.1016/s0300-483x(00)00188-8.
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Chemical reactivity, cytotoxicity, and mutagenicity of chloropropanones.氯丙酮的化学反应性、细胞毒性和致突变性。
Toxicol Appl Pharmacol. 1987 Oct;91(1):46-54. doi: 10.1016/0041-008x(87)90192-x.
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Mutat Res. 2007 Nov-Dec;636(1-3):178-242. doi: 10.1016/j.mrrev.2007.09.001. Epub 2007 Sep 12.
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Drinking water disinfection byproducts: review and approach to toxicity evaluation.饮用水消毒副产物:综述与毒性评估方法
Environ Health Perspect. 1999 Feb;107 Suppl 1(Suppl 1):207-17. doi: 10.1289/ehp.99107s1207.
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Pentane as an index of in vitro lipid peroxidation via microsomal NADPH-P-450 enzyme systems.通过微粒体NADPH - P - 450酶系统,戊烷作为体外脂质过氧化的一个指标。
Hiroshima J Med Sci. 1989 Sep;38(3):131-4.
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Evaluating the similarity of complex drinking-water disinfection by-product mixtures: overview of the issues.评估复杂饮用水消毒副产物混合物的相似性:问题概述
J Toxicol Environ Health A. 2009;72(7):429-36. doi: 10.1080/15287390802608890.
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White butterfly (Clerodendrum volubile) leaf extract protects against carbon tetrachloride-induced hepatotoxicity in rats.白花丹(Clerodendrum volubile)叶提取物可预防四氯化碳诱导的大鼠肝毒性。
Biomed Pharmacother. 2017 Dec;96:924-929. doi: 10.1016/j.biopha.2017.12.005. Epub 2017 Dec 7.

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Pharmacol Rev. 1984 Jun;36(2 Suppl):25S-33S.
10
2-Propanol treatment induces selectively the metabolism of carbon tetrachloride to phosgene. Implications for carbon tetrachloride hepatotoxicity.2-丙醇处理选择性地诱导四氯化碳代谢为光气。对四氯化碳肝毒性的影响。
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