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暴露于100%氧气24小时后的大鼠肺葡萄糖代谢。

Rat lung glucose metabolism after 24 h of exposure to 100% oxygen.

作者信息

Bassett D J, Bowen-Kelly E, Reichenbaugh S S

机构信息

Department of Environmental Health Sciences, Johns Hopkins University, School of Hygiene and Public Health, Baltimore, Maryland 21205.

出版信息

J Appl Physiol (1985). 1989 Feb;66(2):989-96. doi: 10.1152/jappl.1989.66.2.989.

Abstract

Previous studies with lung homogenates and isolated cells have suggested oxygen cell injury results from the inhibition of key enzymes involved in both cytosolic and mitochondrial energy generation. In this study, the extent and pattern of metabolism of D-[U-14C, 5-3H]glucose was examined in perfused lungs isolated from rats before and after 24 h of in vivo exposure to 100% O2. Lung ATP levels after O2 exposure were maintained by a 53% increase in glucose utilization from an unexposed control value of 18.0 +/- 3.2 to 27.5 +/- 3.0 mumol 3H2O.h-1.g dry wt-1, accounted for by an enhanced rate of lactate plus pyruvate production from 15.7 +/- 2.0 to 32.7 +/- 4.1 mumol.h-1.g dry wt-1 with no alteration in lactate-to-pyruvate ratio. CO2 production was unaltered from a control rate of 27.5 +/- 4.0 14CO2 mumol.h-1.g dry wt-1. Maximal rates of glucose metabolism were determined by perfusion with 0.8 mM dinitrophenol, giving for air-exposed lungs a rate of 53.5 +/- 5.0 mumol 3H2O.h-1.g dry wt-1 and increased lactate plus pyruvate and 14CO2 production rates of 46.5 +/- 6.5 and 128.3 +/- 19.6 mumol.h-1.g dry wt-1, respectively. Although this maximal rate of glucose utilization was unaltered in oxygen-exposed lungs, lactate plus pyruvate production was further increased to 80.0 +/- 9.1 mumol.h-1.g dry wt-1 with a concomitant decrease in the dinitrophenol-induced rate of 14CO2 production to 81.5 +/- 9.2 mumol.h-1.g dry wt-1.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

先前对肺匀浆和分离细胞的研究表明,氧细胞损伤是由于参与胞质和线粒体能量生成的关键酶受到抑制所致。在本研究中,检测了从大鼠体内分离的灌注肺在体内暴露于100%氧气24小时前后D-[U-14C, 5-3H]葡萄糖的代谢程度和模式。氧气暴露后肺ATP水平得以维持,葡萄糖利用率从未暴露对照组的18.0±3.2增加53%至27.5±3.0μmol 3H2O·h-1·g干重-1,这是由于乳酸加丙酮酸生成速率从15.7±2.0增加至32.7±4.1μmol·h-1·g干重-1,而乳酸与丙酮酸的比率未改变。二氧化碳生成量与对照组27.5±4.0μmol 14CO2·h-1·g干重-1的速率无差异。通过用0.8 mM二硝基苯酚灌注来测定葡萄糖代谢的最大速率,对于空气暴露的肺,速率为53.5±5.0μmol 3H2O·h-1·g干重-1,乳酸加丙酮酸和14CO2生成速率分别增加至46.5±6.5和128.3±19.6μmol·h-1·g干重-1。尽管在氧气暴露的肺中这种葡萄糖利用的最大速率未改变,但乳酸加丙酮酸生成进一步增加至80.0±9.1μmol·h-1·g干重-1,同时二硝基苯酚诱导的14CO2生成速率降至81.5±9.2μmol·h-1·g干重-1。(摘要截断于250字)

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