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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/L809    most recent 00448.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Merker, M. P. Articles by Bongard, R. D. Search for Related Content PubMed PubMed Citation Articles by Merker, M. P. Articles by Bongard, R. D.

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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