title: Pulmonary arterial endothelial cells affect the redox status of coenzyme Q0.
abstract: The pulmonary endothelium is capable of reducing certain redox-active compounds as they pass from the systemic venous to the arterial circulation. This may have important consequences with regard to the pulmonary and systemic disposition and biochemistry of these compounds. Because quinones comprise an important class of redox-active compounds with a range of physiological, toxicological, and pharmacological activities, the objective of the present study was to determine the fate of a model quinone, coenzyme Q0 (Q), added to the extracellular medium surrounding pulmonary arterial endothelial cells in culture, with particular attention to the effect of the cells on the redox status of Q in the medium. Spectrophotometry, electron paramagnetic resonance (EPR), and high-performance liquid chromatography (HPLC) demonstrated that, when the oxidized form Q is added to the medium surrounding the cells, it is rapidly converted to its quinol form (QH2) with a small concentration of semiquinone (Q*-) also detectable. The isolation of cell plasma membrane proteins revealed an NADH-Q oxidoreductase located on the outer plasma membrane surface, which apparently participates in the reduction process. In addition, once formed the QH2 undergoes a cyanide-sensitive oxidation by the cells. Thus, the actual rate of Q reduction by the cells is greater than the net QH2 output from the cells.
authors.affiliation: Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA.
authors.forename: Said H
authors.initials: SH
authors.lastname: Audi
authors.forename: Hongtao
authors.initials: H
authors.lastname: Zhao
authors.forename: Robert D
authors.initials: RD
authors.lastname: Bongard
authors.forename: Neil
authors.initials: N
authors.lastname: Hogg
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Kettenhofen
authors.forename: Balaraman
authors.initials: B
authors.lastname: Kalyanaraman
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Dawson
authors.forename: Marilyn P
authors.initials: MP
authors.lastname: Merker
mesh_terms: D000818:Animals; D001158:Arteries / Q000166:cytology*; D001710:Biotin / Q000494:pharmacology; D019921:Biotinylation; D002417:Cattle; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D002851:Chromatography, High Pressure Liquid; D004305:Dose-Response Relationship, Drug; D004578:Electron Spin Resonance Spectroscopy; D004583:Electrons; D004730:Endothelium, Vascular / Q000378:metabolism*; D005609:Free Radicals; D008168:Lung / Q000166:cytology*; D008956:Models, Chemical; D009249:NADP; D010084:Oxidation-Reduction; D013997:Time Factors; D014451:Ubiquinone / Q000378:metabolism*
chemical_list: D005609:Free Radicals; D014451:Ubiquinone; D009249:NADP; D001710:Biotin