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间歇性缺氧可减少大鼠肝细胞复氧过程中氧自由基的形成。

Intermittent anoxia reduces oxygen free radicals formation during reoxygenation in rat hepatocytes.

作者信息

Gasbarrini A, Colantoni A, Di Campli C, De Notariis S, Masetti M, Iovine E, Mazziotti A, Massari I, Gasbarrini G, Pola P, Bernardi M

机构信息

Catholic University of Roma, Italy.

出版信息

Free Radic Biol Med. 1997;23(7):1067-72. doi: 10.1016/s0891-5849(97)00141-x.

Abstract

The sensitivity of liver cells to anoxia is a major problem afflicting liver preservation and transplantation. Intermittent ischemia has been proposed to reduce reperfusion injury. The aim of the study was to assess oxygen free radical formation and cell injury during continuous or intermittent anoxia/reoxygenation in rat hepatocytes. Anion superoxide was measured by lucigenin-enhanced chemiluminescence and cell damage by LDH release and trypan blue uptake. During anoxia, superoxide generation dropped to background level in both groups; trypan blue uptake and LDH release, which increased progressively, were significantly greater in hepatocytes exposed to continuous compared to intermittent anoxia. During reoxygenation, a massive generation of superoxide anion formation, followed by a sharp increase in LDH release, was observed in both groups. However, both oxyradical generation and cell injury were significantly greater in cells exposed to continuous compared to intermittent anoxia. The data, showing that intermittent oxygen deprivation reduce liver cell injury and oxygen free radical formation determined by anoxia/reoxygenation, suggest a novel possible approach to the reduction of reperfusion injury.

摘要

肝细胞对缺氧的敏感性是困扰肝脏保存和移植的一个主要问题。间歇性缺血被认为可以减少再灌注损伤。本研究的目的是评估大鼠肝细胞在持续或间歇性缺氧/复氧过程中氧自由基的形成和细胞损伤情况。通过光泽精增强化学发光法测定超氧阴离子,通过乳酸脱氢酶(LDH)释放和台盼蓝摄取来检测细胞损伤。在缺氧期间,两组中超氧阴离子的产生均降至背景水平;与间歇性缺氧相比,持续缺氧的肝细胞中台盼蓝摄取和LDH释放逐渐增加,且显著更高。在复氧期间,两组均观察到超氧阴离子大量生成,随后LDH释放急剧增加。然而,与间歇性缺氧相比,持续缺氧的细胞中氧自由基生成和细胞损伤均显著更大。这些数据表明,间歇性缺氧可减少由缺氧/复氧所决定的肝细胞损伤和氧自由基形成,提示了一种减少再灌注损伤的新的可能方法。

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