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正己烷可诱导啮齿动物患帕金森症。

n-hexane induces parkinsonism in rodents.

作者信息

Pezzoli G, Ricciardi S, Masotto C, Mariani C B, Carenzi A

机构信息

Ospedale Maggiore Policlinico, University of Milan, Italy.

出版信息

Brain Res. 1990 Oct 29;531(1-2):355-7. doi: 10.1016/0006-8993(90)90801-h.

Abstract

A case of human parkinsonism, due to n-hexane exposure, was recently described. On the basis of this observation, we treated mice and rats with n-hexane and its principle toxic metabolite 2,5-hexanedione. The mice underwent a chronic treatment intraperitoneum, the rats were treated stereotaxically into the substantia nigra. At biochemical analysis of the striata, dopamine and homovanillic acid levels were significantly lower compared with control animals; norepinephrine, serotonin, 5-hydroxindolacetic acid levels were unchanged. The rats treated with 2,5-hexanedione showed an apomorphine-induced rotational behavior significantly higher compared to controls. Since n-hexane and its metabolites are environmental contaminants and by-products of endogenous metabolic pathways, we propose that they may play a role in inducing parkinsonism in humans.

摘要

最近报道了一例因接触正己烷而导致人类帕金森症的病例。基于这一观察结果,我们用正己烷及其主要有毒代谢产物2,5 - 己二酮对小鼠和大鼠进行了处理。小鼠接受腹腔内慢性处理,大鼠通过立体定向注射至黑质。在对纹状体进行生化分析时,与对照动物相比,多巴胺和高香草酸水平显著降低;去甲肾上腺素、血清素、5 - 羟吲哚乙酸水平未发生变化。用2,5 - 己二酮处理的大鼠与对照组相比,阿扑吗啡诱导的旋转行为明显更高。由于正己烷及其代谢产物是环境污染物和内源性代谢途径的副产物,我们认为它们可能在诱发人类帕金森症中发挥作用。

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