黄嘌呤氧化酶增加并促成百草枯诱导的急性肺损伤。

Xanthine oxidase is increased and contributes to paraquat-induced acute lung injury.

作者信息

Waintrub M L, Terada L S, Beehler C J, Anderson B O, Leff J A, Repine J E

机构信息

Webb-Waring Lung Institute, Department of Medicine, University of Colorado, Health Sciences Center, Denver 80262.

出版信息

J Appl Physiol (1985). 1990 Apr;68(4):1755-7. doi: 10.1152/jappl.1990.68.4.1755.

DOI:10.1152/jappl.1990.68.4.1755

PMID:2347813

Abstract

Two lines of investigation suggested that xanthine oxidase- (XO) derived O2 metabolites contribute to paraquat- (PQ) induced acute lung injury. First, PQ treatment increased lung XO activity and decreased lung xanthine dehydrogenase activity. Second, lung albumin uptake increased compared with control values in untreated XO-replete but not tungsten-treated XO-depleted lungs in rats treated with PQ.

摘要

两条研究线索表明，黄嘌呤氧化酶（XO）衍生的氧代谢产物促成了百草枯（PQ）诱导的急性肺损伤。第一，PQ处理增加了肺XO活性，并降低了肺黄嘌呤脱氢酶活性。第二，在用PQ处理的大鼠中，与未处理的XO充足的对照值相比，肺白蛋白摄取增加，但在钨处理的XO缺乏的肺中则不然。