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首页> 外文期刊>Journal of applied toxicology >Aluminum phosphide poisoning: an unsolved riddle
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Aluminum phosphide poisoning: an unsolved riddle

机译：磷化铝中毒：一个未解之谜

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Aluminum phosphide (ALP), a widely used insecticide and rodenticide, is also infamous for the mortality and morbidity it causes in ALP-poisoned individuals. The toxicity of metal phosphides is due to phosphine liberated when ingested phosphides come into contact with gut fluids. ALP poisoning is lethal, having a mortality rate in excess of 70%. Circulatory failure and severe hypotension are common features of ALP poisoning and frequent cause of death. Severe poisoning also has the potential to induce multi-organ failure. The exact site or mechanism of its action has not been proved in humans. Rather than targeting a single organ to cause gross damage, ALP seems to work at the cellular level, resulting in widespread damage leading to multiorgan dysfunction (MOD) and death. There has been proof in vitro that phosphine inhibits cytochrome c oxidase. However, it is unlikely that this interaction is the primary cause of its toxicity. Mitochondria could be the possible site of maximum damage in ALP poisoning, resulting in low ATP production followed by metabolic shutdown and MOD; also, owing to impairment in electron flow, there could be free radical generation and damage, again producing MOD. Evidence of reactive oxygen species-induced toxicity owing to ALP has been observed in insects and rats. A similar mechanism could also play a role in humans and contribute to the missing link in the pathogenesis of ALP toxicity. There is no specific antidote for ALP poisoning and supportive measures are all that are currently available.
机译：磷化铝（ALP）是一种广泛使用的杀虫剂和灭鼠剂，它因ALP中毒而导致的死亡率和发病率也是臭名昭著的。金属磷化物的毒性是由于摄入的磷化物与肠液接触会释放出磷化氢。 ALP中毒具有致命性，死亡率超过70％。循环衰竭和严重的低血压是ALP中毒的常见特征，也是常见的死亡原因。严重中毒还可能诱发多器官衰竭。其作用的确切部位或机制尚未在人类中得到证实。 ALP似乎不是针对单个器官造成严重伤害，而是在细胞水平上起作用，从而导致广泛的伤害，从而导致多器官功能障碍（MOD）和死亡。体外已证明膦可抑制细胞色素c氧化酶。但是，这种相互作用不太可能是其毒性的主要原因。线粒体可能是ALP中毒最大破坏的可能部位，导致ATP产量低，随后发生代谢性关闭和MOD。同样，由于电子流的损害，可能会产生自由基并造成破坏，再次产生MOD。已经在昆虫和大鼠中观察到由于ALP引起的活性氧引起的毒性的证据。类似的机制也可能在人类中发挥作用，并导致ALP毒性发病机理中的缺失环节。目前尚无针对ALP中毒的专门解毒剂，并且目前提供所有支持措施。

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