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大鼠肺和心脏对85%氧气适应性反应的时间进程及定量分析。

Time course and quantitative analysis of the adaptive responses to 85% oxygen in the rat lung and heart.

作者信息

Evelson P, González-Flecha B

机构信息

Physiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave., MA 02115, Boston, USA.

出版信息

Biochim Biophys Acta. 2000 Oct 18;1523(2-3):209-16. doi: 10.1016/s0304-4165(00)00124-0.

Abstract

The phenomenon of oxygen tolerance (resistance to 100% O(2) in rats previously exposed to 85% O(2)) constitutes one of the few models of adaptive responses to oxidative stress in mammals. In vitro studies suggest that reactive oxygen species mediate this response. To test this hypothesis in vivo, we followed the time course of oxidative stress, enzyme induction, and edema in the lung, heart and liver of rats exposed to 85% O(2) for 1 to 5 days. Interestingly, not only the lung, but also the heart of rats exposed to 85% O(2) showed increases in the production of O(-)(2) (aconitase inactivation) early during the exposure. Increases in O(-)(2) were associated to oxidative stress (increased in situ chemiluminescence) and transient edema in both tissues. Both the lung and heart displayed induction of superoxide dismutase and reversion of the oxidative stress and damage. The adaptive response in the heart was faster and more efficient, suggesting that this tissue is at a more critical risk when exposed to elevated O(2) concentrations.

摘要

氧耐受现象(先前暴露于85%氧气环境中的大鼠对100%氧气具有抗性)是哺乳动物对氧化应激适应性反应的少数模型之一。体外研究表明,活性氧介导了这种反应。为了在体内验证这一假设,我们追踪了暴露于85%氧气环境1至5天的大鼠肺、心脏和肝脏中氧化应激、酶诱导和水肿的时间进程。有趣的是,不仅肺,暴露于85%氧气环境的大鼠心脏在暴露早期也显示超氧阴离子(O₂⁻)生成增加(乌头酸酶失活)。O₂⁻增加与两种组织中的氧化应激(原位化学发光增加)和短暂性水肿相关。肺和心脏均表现出超氧化物歧化酶的诱导以及氧化应激和损伤的逆转。心脏中的适应性反应更快且更有效,表明该组织在暴露于高浓度氧气时面临更高的风险。

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