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Oxygen toxicity from plants to people

机译:植物对人的氧气毒性

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Over the past 30 years, acute oxygen toxicity in plants, mammals and enteric bacteria has been defined in terms of specific interactions of oxygen with a limited number of molecular targets. At least in the case of plants and mammals, response at the level of the whole organism is a consequence of oxygen's interaction with enzymes that should not exhibit oxygen sensitivity, ribulose-1,5-bisphosphate carboxylase/oxygenase (rubisco) and glutamate decarboxylase (GAD). In enteric bacteria, inhibition of acetolactate synthase (ALS), or the production of peracetic acid by this enzyme, may be a contributing factor in the inactivation of dihydroxyacid dehydratase and loss of the ability to synthesize branched-chain amino acids under conditions of hyperbaric oxygen. The facile interaction of these enzymes with oxygen has questioned our fundamental understanding of their reaction mechanisms. Could these enzymes have radical mechanisms?
机译:在过去的30年中,根据氧气与有限数量的分子靶标的特异性相互作用,已经定义了植物,哺乳动物和肠道细菌的急性氧气毒性。至少在植物和哺乳动物的情况下,整个生物体水平的反应是氧气与不应表现出对氧气敏感的酶,核糖-1,5-双磷酸羧化酶/加氧酶(rubisco)和谷氨酸脱羧酶( GAD)。在肠细菌中,抑制乙酰乳酸合酶(ALS)或由该酶产生过氧乙酸可能是导致二羟酸脱水酶失活和在高压氧条件下丧失合成支链氨基酸能力的因素。这些酶与氧气的简便相互作用已经质疑了我们对其反应机理的基本理解。这些酶可能具有自由基机制吗?

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