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A yeast mutant lacking mitochondrial manganese-superoxide dismutase is hypersensitive to oxygen.

机译:缺乏线粒体锰超氧化物歧化酶的酵母突变体对氧气过敏。

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摘要

The nuclear gene for manganese-containing superoxide dismutase (MnSOD; superoxide:superoxide oxidoreductase, EC 1.15.1.1) of yeast mitochondria was mapped on chromosome VIII and inactivated by gene disruption. The resulting mutant lacked any protein cross-reacting with anti-MnSOD antibodies, and its mitochondria exhibited less than 1% of the cyanide-insensitive superoxide dismutase activity found in mitochondria of the wild-type parent strain. In the absence of oxygen, the mutant grew as rapidly as the wild-type parent. However, increasing concentrations of oxygen led to a progressive inhibition of growth. The properties of this mutant provide direct evidence that MnSOD contributes to the natural protection of cells against oxygen toxicity.
机译:酵母线粒体的含锰超氧化物歧化酶(MnSOD;超氧化物:超氧化物氧化还原酶,EC 1.15.1.1)的核基因被定位在VIII染色体上,并因基因破坏而失活。所得突变体缺乏与抗MnSOD抗体发生交叉反应的任何蛋白质,其线粒体的野生型亲本菌株线粒体中氰化物不敏感的超氧化物歧化酶活性不足1%。在没有氧气的情况下,突变体的生长速度与野生型亲本一样快。但是,氧气浓度的增加导致生长的逐步抑制。该突变体的性质提供了直接的证据,即MnSOD有助于自然保护细胞抵抗氧中毒。

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