文航华,张希洲.NO在百草枯中毒中的作用机制研究新进展[J].内科急危重症杂志,2016,22(2):
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| 中文关键词: 一氧化氮 一氧化氮合酶 百草枯中毒 |
| 英文关键词:NO NOS paraquat poisoning |
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| 中文摘要: |
| 【摘要】百草枯（Paraquat PQ）是一种阳离子接触性除草剂，摄入人体后能引起肺及神经系统的退行性变及多脏器的损伤。尽管百草枯中毒的确切机制尚未定论，由氧化还原反应导致还原当量的减少以及超氧阴离子的产生是百草枯中毒的关键环节已成为共识。还原当量的减少会极大的影响NADPH相关生理化学机能。超氧阴离子的产生会诱导大量的活性氧（ROS）与细胞内大分子物质反应。NO在PQ中毒过程中发挥着重要的作用，它可以与超氧化物反应生成亚硝酸盐导致细胞损伤。还可以介导其它信号通路的的传递,参与到氧化与抗氧化反应中。NO在百草枯中毒过程中作用已经得到实验证实，但是对于NO的具体效应，目前仍有争议。本文通过总结近十几年来的研究发现，总结出NO在PQ中毒过程中主导的可能作用机制。 |
| 英文摘要: |
| The mechanisms of NO in paraquat poisoning latest developments
【Abstract】Paraquat (1,1’-dimethyl-4,4’-bipyridinium dichloride) is a nonselective and contact herbicide used worldwide and cause high mortality rate (more than 80%) after accidental or deliberate self-poisoning. The pathogenesis of paraquat toxicity consists of two distinct phases. The initial stage involves acute damage to several organs and death may occur during this period and is associated with pulmonary , renal and circulatory failure. Patients surviving this stage may evolve to the second stage, which is characterized by damage almost exclusively to the lungs. Extensive pulmonary fibrosis ensues, resulting in death from respiratory failure. |
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