Early Decrease in Rotenone‐Sensitive Coenzyme Q1 Reduction in Intact Lungs From Rats Exposed to Hyperoxia

The objective of this study was to evaluate biochemical changes in lung tissue that may precede the gross lung structural and hemodynamic changes associated with exposure to hyperoxia (85% O 2 ) for > 3 days. We measured the rate of appearance of the hydroquinone form (CoQ 1 H 2 ) of coenzyme Q 1 (CoQ 1 ) in the venous effluent during CoQ 1 infusion at different concentrations into the pulmonary artery of isolated perfused lungs from adult rats exposed to either room air (normoxic) or 85% O 2 (hyperoxic) for 48 hrs. Kinetic analysis of the data revealed that hyperoxia decreased the maximum rate of CoQ 1 H 2 appearance in the venous effluent (V max ) from 9.35 ± 0.42 (SE) μmol/min/g dry lung wt for normoxic lungs (n = 6) to 7.62 ± 0.23 for hyperoxic lungs (n = 6), with no effect on lung wet weight, wet‐to‐dry weight ratio or pulmonary artery pressure. Lung perfusion with rotenone (20 μM), an inhibitor of mitochondrial complex I, decreased V max values to 5.77 ± 0.63 for normoxic lungs (n = 4) and 5.85 ± 0.17 for hyperoxic lungs (n = 4). These V max values for rotenone‐insensitive CoQ 1 reduction in normoxic and hyperoxic lungs are not significantly different. These results suggest that rat exposure to hyperoxia for 48 hrs decreases rotenone sensitive lung CoQ 1 reductase activity by ~ 50% and that this decrease is a potential early index of hyperoxia‐induced pulmonary oxidative stress. Support: HL‐24349, HL‐65537, and Dept. of Veterans’ Affairs.