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四氯化碳和三氯溴甲烷的毒性。代谢裂解产物的共价结合和脂质过氧化在微粒体钙隔离抑制中的双重作用。

Carbon tetrachloride and bromotrichloromethane toxicity. Dual role of covalent binding of metabolic cleavage products and lipid peroxidation in depression of microsomal calcium sequestration.

作者信息

Waller R L, Glende E A, Recknagel R O

出版信息

Biochem Pharmacol. 1983 May 15;32(10):1613-7. doi: 10.1016/0006-2952(83)90336-2.

DOI:10.1016/0006-2952(83)90336-2
PMID:6860348
Abstract

We have investigated the importance of covalent binding and lipid peroxidation on the depression of microsomal calcium sequestration associated with in vitro metabolism of 14CCl4. Studies with CBrCl3 are also reported. In aerobic systems, promethazine was used to block lipid peroxidation, measured as malondialdehyde (MDA) generation. Effects of low levels of lipid peroxidation were tested in Fe2+-supplemented systems free of halogenated hydrocarbons. The results indicate that microsomal calcium sequestration can be depressed significantly by metabolism of either CCl4 or CBrCl3 in the absence of MDA generation, or by lipid peroxidation occurring in the absence of halogenated hydrocarbons.

摘要

我们研究了共价结合和脂质过氧化作用对与四氯化碳体外代谢相关的微粒体钙隔离抑制的重要性。还报告了用三氯溴甲烷进行的研究。在需氧系统中,用异丙嗪来阻断脂质过氧化作用,脂质过氧化作用以丙二醛(MDA)生成量来衡量。在不含卤代烃的亚铁离子补充系统中测试了低水平脂质过氧化作用的影响。结果表明,在没有丙二醛生成的情况下,四氯化碳或三氯溴甲烷的代谢,或者在没有卤代烃的情况下发生的脂质过氧化作用,均可显著抑制微粒体钙隔离。

相似文献

1
Carbon tetrachloride and bromotrichloromethane toxicity. Dual role of covalent binding of metabolic cleavage products and lipid peroxidation in depression of microsomal calcium sequestration.四氯化碳和三氯溴甲烷的毒性。代谢裂解产物的共价结合和脂质过氧化在微粒体钙隔离抑制中的双重作用。
Biochem Pharmacol. 1983 May 15;32(10):1613-7. doi: 10.1016/0006-2952(83)90336-2.
2
Inhibition of Ca2+ sequestration in foetal liver microsomes by carbon tetrachloride and bromotrichloromethane.
Biochem Pharmacol. 1984 Aug 15;33(16):2605-8. doi: 10.1016/0006-2952(84)90632-4.
3
Rapid depression of rat liver microsomal calcium pump activity after administration of carbon tetrachloride or bromotrichloromethane and lack of effect after ethanol.
Toxicol Appl Pharmacol. 1981 Jun 30;59(2):389-94. doi: 10.1016/0041-008x(81)90210-6.
4
Carbon tetrachloride, bromotrichloromethane and ethanol acute intoxication. New chemical evidence for lipid peroxidation in rat tissue microsomes.四氯化碳、三氯溴甲烷和乙醇急性中毒。大鼠组织微粒体脂质过氧化的新化学证据。
Biochem J. 1983 Jun 15;212(3):625-31. doi: 10.1042/bj2120625.
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Destruction of microsomal calcium pump activity: a possible secondary mechanism in BrCCl3 and CCl4 liver cell injury.
Adv Exp Med Biol. 1981;136 Pt A:619-31. doi: 10.1007/978-1-4757-0674-1_45.
6
Promethazine inhibits the formation of aldehydic products of lipid peroxidation but not covalent binding resulting from the exposure of rat liver fractions to CCl4.异丙嗪可抑制脂质过氧化醛类产物的形成,但不能抑制大鼠肝匀浆暴露于四氯化碳时产生的共价结合。
Biochem J. 1989 Dec 1;264(2):527-32. doi: 10.1042/bj2640527.
7
Promethazine administration to rats and CCl4 induced lipid peroxidation of liver microsomal lipids.给大鼠注射异丙嗪以及使用四氯化碳会诱导肝微粒体脂质的脂质过氧化。
Res Commun Chem Pathol Pharmacol. 1980 Oct;30(1):91-8.
8
Oxidation of carbon tetrachloride, bromotrichloromethane, and carbon tetrabromide by rat liver microsomes to electrophilic halogens.大鼠肝脏微粒体将四氯化碳、三氯溴甲烷和四溴化碳氧化为亲电卤素。
Life Sci. 1982 Jan 11;30(2):131-7. doi: 10.1016/0024-3205(82)90644-0.
9
The formation of diglutathionyl dithiocarbonate as a metabolite of chloroform, bromotrichloromethane, and carbon tetrachloride.作为氯仿、溴三氯甲烷和四氯化碳代谢产物的二谷胱甘肽二硫代碳酸酯的形成。
Drug Metab Dispos. 1981 Jul-Aug;9(4):334-9.
10
Relationship of oxygen and glutathione in protection against carbon tetrachloride-induced hepatic microsomal lipid peroxidation and covalent binding in the rat. Rationale for the use of hyperbaric oxygen to treat carbon tetrachloride ingestion.氧气与谷胱甘肽在保护大鼠免受四氯化碳诱导的肝微粒体脂质过氧化及共价结合中的关系。使用高压氧治疗四氯化碳摄入的理论依据。
J Clin Invest. 1984 Dec;74(6):1996-2001. doi: 10.1172/JCI111621.

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