氯甲烷的行为、神经和毒性作用:文献综述。

J D Repko, S M Lasley
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引用次数: 33

摘要

大量的报告致力于氯甲烷的生理和毒性作用,其中许多是基于涉及职业接触的病例史。氯甲烷对中枢和周围神经系统的有害作用是公认的。它是一种中度严重的麻醉剂和潜在严重的神经毒药。慢性中毒与中枢神经系统(CNS)、肾脏、肝脏、骨髓、心血管系统、呼吸系统和肠道的损害有关。体征和症状范围从较严重的医学功能障碍,如心脏不规则、呼吸麻痹、神经变性和严重抽搐,到较细微的临床观察,如中枢神经系统抑制、神经紧张和情绪不稳定、失眠和厌食症、共济失调、视力模糊、头晕、恶心、头晕、麻醉和定向障碍。这些和其他氯甲烷神经毒性作用的行为相关性表明,行为退化是逐渐发生的。药效学研究表明,该化合物可迅速被血液吸收,大多数作者将其毒性归因于体内酶催化的甲基化反应。尽管有几位研究人员试图将氯甲烷的这种生物反应与其毒性联系起来,但目前对这一问题的了解仍然缺乏详细的作用机制。在这些机制得到证实之前,必须有效地开发评估亚临床神经和行为变化的适当方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Behavioral, neurological, and toxic effects of methyl chloride: a review of the literature.

A large number of reports have been devoted to the physiologic and toxic effects of methyl chloride, many of which are based on case histories involving occupational exposure. The detrimental actions of methyl chloride on the central and peripheral nervous systems are well established effects. It is a moderately severe narcotic and potentially severe nerve poison. Chronic intoxication is associated with damage to the central nervous system (CNS), kidneys, liver, bone marrow, cardiovascular system, respiratory system, and intestinal tract. The signs and symptoms range from the more severe medical dysfunctions such as cardiac irregularities, respiratory paralysis, nerve degeneration, and severe convulsions to the more subtle clinical observations such as CNS depression, nervousness and emotional instability, insomnia and anorexia, ataxia, blurred vision, light-headedness, nausea, dizziness, narcosis, and disorientation. The behavioral correlates of these and other neurotoxic effects of methyl chloride suggest that a gradual behavioral degradation occurs. Pharmacodynamic studies have shown the compound to be rapidly absorbed by the blood with most authors attributing the toxicity to an enzyme-catalyzed methylation reaction in the body. Despite the fact that several investigators have attempted to correlate such biological responses of methyl chloride with its toxicity, the present knowledge of the problem still lacks a detailed mechanism of action. Until such mechanisms are verified, adequate methods to assess subclinical neurological and behavioral changes must be effectively developed.

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