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Pulmonary and Critical Care Medicine, 4

By Said H. Audi, Robert D. Bongard, Gary S. Krenz, David A. Rickaby, Steven T, Jessica Eisenhauer, David L. Roerig and Marilyn P. Merker

Abstract

NAD(P)H:quinone oxidoreductase (NQO1) plays a dominant role in the reduction of the quinone compound 2,3,5,6-tetramethyl-1,4-benzoquinone (duroquinone, DQ) to durohydroquinone (DQH2) on passage through the rat lung. Exposure of adult rats to sublethal hyperoxia (85 % O2) for seven or more days stimulates adaptation to the otherwise lethal effects of> 95 % O2. The objective of this study was to examine whether exposure of adult rats to hyperoxia (85 % O2 for 48 hours or 21 days) affected lung NQO1 activity as measured by the rate of DQ reduction on passage through the lung. We measured the appearance of DQH2 in the venous effluent during DQ infusion at different concentrations into the pulmonary artery of isolated perfused lungs from rats that had been exposed to room air or to 85 % O2. We also evaluated the effect of hyperoxia on vascular transit time distribution, and measured NQO1 activity and protein in lung homogenate. The results demonstrate that exposure to 85 % O2 for 21 days increases lung capacity to reduce DQ to DQH2, and that NQO1 is the dominant DQ reductase in normoxic and hyperoxic lungs. Kinetic analysis revealed that 21 day hyperoxia exposure increased the maximum rate of pulmonary DQ reduction, Vmax, from 1.95 ± 0.14 (SE) t

Year: 2013
OAI identifier: oai:CiteSeerX.psu:10.1.1.326.6412
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