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新生大鼠对常压高氧耐受性的推测机制。

Proposed mechanism for neonatal rat tolerance to normobaric hyperoxia.

作者信息

Stevens J B, Autor A P

出版信息

Fed Proc. 1980 Nov;39(13):3138-43.

PMID:6253331
Abstract

Induction of two forms of superoxide dismutase, catalase and glutathione peroxidase, occurs very rapidly in neonatal rat lung tissue upon exposure of these animals to 94 + % normobaric oxygen. No such oxygen-mediated enzyme induction occurs in the lungs of adult rats. The aged-dependent pattern of enzyme induction correlates with the well-established age-dependent tolerance of neonatal rats to hyperoxia. Enzyme induction occurs in the lungs of neonates in only those species known to be resistant to oxygen-provoked lung damage. Compromise of oxygen-mediated enzyme induction predisposed the neonatal rats to pulmonary oxygen toxicity. These data have formed the basis of the proposal that oxygen induction of the superoxide dismutases catalase and glutathione peroxidase provides a vital part of the defense mechanism against oxygen toxicity. A biochemical mechanism of oxygen-provoked pulmonary damage has been elaborated to explain the role of each enzyme in the protection against oxygen and free radical toxicity.

摘要

当新生大鼠暴露于94%以上的常压氧气中时,其肺组织中两种形式的超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的诱导反应非常迅速。成年大鼠的肺中不会发生这种由氧气介导的酶诱导反应。酶诱导的年龄依赖性模式与新生大鼠对高氧已确立的年龄依赖性耐受性相关。只有在已知对氧引发的肺损伤具有抗性的物种中,新生动物的肺中才会发生酶诱导反应。氧介导的酶诱导反应受损使新生大鼠易患肺氧中毒。这些数据构成了以下提议的基础:超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的氧诱导反应是对抗氧毒性防御机制的重要组成部分。已经阐述了氧引发的肺损伤的生化机制,以解释每种酶在抵御氧和自由基毒性中的作用。

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