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产前一氧化碳暴露的神经毒性。

Neurotoxicity of prenatal carbon monoxide exposure.

作者信息

Fechter L D

机构信息

Department of Environmental Health Sciences, Johns Hopkins University.

出版信息

Res Rep Health Eff Inst. 1987 Sep(12):3-22.

PMID:3269253
Abstract

Despite the very wide recognition that carbon monoxide (CO) is a significant neurotoxicant, the level at which subtle effects occur, and the existence of sensitive periods in development for such toxicity, has been undetermined. In terms of risk to the fetus, a potentially susceptible sub-population, there is concern, first, that the level of exposure at which neurotoxicity occurs may be different from the adult, and second, that the site of toxic action and subsequent neurotoxic effects of CO may be different in the immature and mature brain. The investigator studied the susceptibility of the developing brain to moderate levels of CO maintained chronically through the period of neuronal proliferation, and into the period of synapse formation. Carbon monoxide may be thought of as both a prototypical hypoxic agent, and a significant public health hazard in its own right. Carbon monoxide is a ubiquitous toxic agent that accounts for large numbers of deaths and significant morbidity in human populations. Subtle neurotoxic effects of this agent may be even more common, but they may go largely undetected, or fail to be associated with CO exposure. We have shown that prenatal CO exposure at moderate levels can produce significant neurotoxic effects in rats. The data obtained from the cerebellum and neostriatum, in particular, suggest that chronic, moderate perinatal CO exposure may disrupt neuronal proliferation and, perhaps, may disrupt certain markers for neurochemical transmission.

摘要

尽管人们普遍认识到一氧化碳(CO)是一种重要的神经毒剂,但尚未确定其产生细微影响的水平以及发育过程中此类毒性的敏感期是否存在。就对胎儿这一潜在易感亚群的风险而言,首先存在的担忧是,发生神经毒性的暴露水平可能与成年人不同,其次,CO在未成熟和成熟大脑中的毒性作用部位及随后的神经毒性效应可能不同。研究人员研究了发育中的大脑在神经元增殖期以及突触形成期长期暴露于中等水平CO时的易感性。一氧化碳既可以被视为典型的缺氧剂,其本身也是一种重大的公共卫生危害。一氧化碳是一种普遍存在的有毒物质,在人群中导致大量死亡和严重发病。这种物质的细微神经毒性作用可能更为常见,但可能大多未被发现,或者未与CO暴露相关联。我们已经表明,中等水平的产前CO暴露会在大鼠中产生显著的神经毒性作用。特别是从小脑和新纹状体获得的数据表明,围产期长期中等水平的CO暴露可能会扰乱神经元增殖,也许还会扰乱神经化学传递的某些标志物。

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