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Role of mitochondrial electron transport complex I in coenzyme Q₁ reduction by intact pulmonary arterial endothelial cells and the effect of hyperoxia

Departments of ¹Anesthesiology, ²Pharmacology and Toxicology, and ³Pulmonary Medicine, Medical College of Wisconsin, Milwaukee; Departments of ⁴Biomedical Engineering and ⁵Mathematics, Statistics and Computer Science, Marquette University, Milwaukee; and ⁶Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin

Submitted 13 November 2006 ; accepted in final form 27 June 2007

The objective was to determine the impact of intact normoxic and hyperoxia-exposed (95% O₂ for 48 h) bovine pulmonary arterial endothelial cells in culture on the redox status of the coenzyme Q₁₀ homolog coenzyme Q₁ (CoQ₁). When CoQ₁ (50 µM) was incubated with the cells for 30 min, its concentration in the medium decreased over time, reaching a lower level for normoxic than hyperoxia-exposed cells. The decreases in CoQ₁ concentration were associated with generation of CoQ₁ hydroquinone (CoQ₁H₂), wherein 3.4 times more CoQ₁H₂ was produced in the normoxic than hyperoxia-exposed cell medium (8.2 ± 0.3 and 2.4 ± 0.4 µM, means ± SE, respectively) after 30 min. The maximum CoQ₁ reduction rate for the hyperoxia-exposed cells, measured using the cell membrane-impermeant redox indicator potassium ferricyanide, was about one-half that of normoxic cells (11.4 and 24.1 nmol·min^–1·mg^–1 cell protein, respectively). The mitochondrial electron transport complex I inhibitor rotenone decreased the CoQ₁ reduction rate by 85% in the normoxic cells and 44% in the hyperoxia-exposed cells. There was little or no inhibitory effect of NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitors on CoQ₁ reduction. Intact cell oxygen consumption rates and complex I activities in mitochondria-enriched fractions were also lower for hyperoxia-exposed than normoxic cells. The implication is that intact pulmonary endothelial cells influence the redox status of CoQ₁ via complex I-mediated reduction to CoQ₁H₂, which appears in the extracellular medium, and that the hyperoxic exposure decreases the overall CoQ₁ reduction capacity via a depression in complex I activity.

quinone; lung

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