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首页> 外文期刊>Iranian journal of medical hypotheses and ideas. >Proposing an antidote for poisonous phosphine in view of mitochondrial electrochemistry facts
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Proposing an antidote for poisonous phosphine in view of mitochondrial electrochemistry facts

机译：鉴于线粒体电化学事实，提出有毒膦的解毒剂

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Metal phosphides in general are potent pesticides that are a common cause of human poisoning. Various salts of phosphides produce highly toxic phosphine in exposure to gastric acid that results in multi-organ damage and death. There is no antidote for phosphine poisoning and most of human poisoned cases do not survive. All we know so far is that phosphine is a mitochondrial toxin that inhibits cellular respiration and induces oxidative stress. Mechanistically, phosphine as a reducing agent interacts with metal ion cofactors at the active site of enzymes and inhibits key enzymes such as cytochrome C oxidase that lead to inhibition of mitochondrial respiration. Phosphine (E0 = ?1.18 V) as a reducing agent gives electrons to cytochrome C oxidase (E0 = +0.29 V). Metal phosphides with lower reduction potential are stronger electron donors and thus stronger poisons. Our hypothesis is that if an electron receiver stronger than cytochrome C oxidase is used then it would compete with cytochrome C oxidase in interaction with phosphine. This competition might prevent or reduce the inhibition of cellular respiration. This idea can be tested in an animal model of phosphine toxicity by monitoring cardiovascular state and measuring the cardiac mitochondrial function.
机译：通常，金属磷化物是有效的农药，是导致人类中毒的常见原因。各种磷酸盐在暴露于胃酸时会产生剧毒的膦，导致多器官损伤和死亡。没有用于磷化氢中毒的解毒剂，大多数中毒的人都无法生存。到目前为止，我们所知道的只是膦是一种线粒体毒素，可抑制细胞呼吸并诱导氧化应激。从机理上讲，作为还原剂的膦与酶的活性位点处的金属离子辅因子相互作用，并抑制导致线粒体呼吸抑制的关键酶（例如细胞色素C氧化酶）。作为还原剂的膦（E0 =约1.18 V）将电子提供给细胞色素C氧化酶（E0 = +0.29 V）。还原电位较低的金属磷化物是较强的电子给体，因此是较强的毒物。我们的假设是，如果使用比细胞色素C氧化酶更强的电子受体，它将与细胞色素C氧化酶竞争，与膦相互作用。这种竞争可能阻止或减少细胞呼吸的抑制。通过监测心血管状态并测量心脏线粒体功能，可以在膦毒性的动物模型中验证这一想法。

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