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黄嘌呤氧化酶在大鼠肝脏缺血/再灌注损伤中的作用。

The role of xanthine oxidase in ischemia/reperfusion damage of rat liver.

作者信息

Frederiks W M, Bosch K S

机构信息

Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, The Netherlands.

出版信息

Histol Histopathol. 1995 Jan;10(1):111-6.

PMID:7756731
Abstract

Oxygen radicals have been proposed to be involved in the induction of liver cell damage during reperfusion after ischemia. The role of xanthine oxidase in this process and the potential of the antioxidant system have been studied in a model of in vivo ischemia of rat liver followed by 1 h reperfusion by the use of enzyme histochemistry. Based on decreased lactate dehydrogenase activity in certain areas of liver parenchyma, cell damage could already be detected at 1 h reperfusion after ischemia. Incubations performed on serial sections showed that the same areas contained decreased activities of xanthine oxidoreductase, xanthine oxidase, catalase and glucose-6-phosphate dehydrogenase. Some individual cells in the undamaged liver parenchyma expressed a very high glucose-6-phosphate dehydrogenase, which suggests that these cells have a good defence against oxidative stress. It is concluded that oxygen radicals derived from xanthine oxidase do not play a decisive role in the induction of cell damage immediately at reperfusion after ischemia. However, it cannot be excluded that xanthine oxidase present in the blood stream can give rise to the development of additional damage later on.

摘要

有观点认为,氧自由基参与了缺血后再灌注期间肝细胞损伤的诱导过程。通过酶组织化学方法,在大鼠肝脏体内缺血1小时后再灌注的模型中,研究了黄嘌呤氧化酶在此过程中的作用以及抗氧化系统的潜力。基于肝实质某些区域乳酸脱氢酶活性的降低,在缺血后1小时再灌注时就已能检测到细胞损伤。对连续切片进行的孵育显示,相同区域的黄嘌呤氧化还原酶、黄嘌呤氧化酶、过氧化氢酶和葡萄糖-6-磷酸脱氢酶活性均降低。未受损肝实质中的一些单个细胞表达出非常高的葡萄糖-6-磷酸脱氢酶,这表明这些细胞对氧化应激具有良好的防御能力。得出的结论是,缺血后再灌注即刻,源自黄嘌呤氧化酶的氧自由基在诱导细胞损伤方面并不起决定性作用。然而,不能排除血流中存在的黄嘌呤氧化酶随后可能导致额外损伤的发生。

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