金属神经毒性的分子机制。

P Nicotera, A Rossi
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引用次数: 0

摘要

最近的流行病学和实验研究表明,某些微量元素(包括金属)的毒性和致癌作用可能达到与在一般环境中接触相适应的水平。尽管大量的研究描述了金属细胞毒性,但所涉及的分子机制仍然知之甚少。然而,现在看来很清楚,几种金属可以与参与信号转导的蛋白质相互作用,包括Ca2+通道和泵。由此导致的细胞对激素和生长因子的刺激作出充分反应的能力受损,导致重要细胞功能的丧失,并最终危及细胞存活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mechanisms of metal neurotoxicity.

Recent epidemiological and experimental research indicates that toxic and carcinogenic effects of certain trace elements including metals may occur at levels compatible with exposure in the general environment. Despite a large number of studies describing metal cytotoxicity, the molecular mechanisms involved are still poorly understood. However, it now appears clear that several metals can interact with proteins involved in signal transduction, including Ca2+ channels and pumps. The resulting impairment of the ability of cells to respond adequately to the stimulation by hormones and growth factors results in the loss of important cell functions and can ultimately compromise cell survival.

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