linoleic-acid and duroquinone

The study objective was to use pulmonary arterial endothelial cells to examine kinetics and mechanisms contributing to the disposition of the quinone 2,3,5,6-tetramethyl-1,4-benzoquinone (duroquinone, DQ) observed during passage through the pulmonary circulation. The approach was to add DQ, durohydroquinone (DQH2), or DQ with the cell membrane-impermeant oxidizing agent, ferricyanide (Fe(CN)6(3)-), to the cell medium, and to measure the medium concentrations of substrates and products over time. Studies were carried out under control conditions and with dicumarol, to inhibit NAD(P)H:quinone oxidoreductase 1 (NQO1), or cyanide, to inhibit mitochondrial electron transport. In control cells, DQH2 appears in the extracellular medium of cells incubated with DQ, and DQ appears when the cells are incubated with DQH2. Dicumarol blocked the appearance of DQH2 when DQ was added to the cell medium, and cyanide blocked the appearance of DQ when DQH2 was added to the cell medium, suggesting that the two electron reductase NQO1 dominates DQ reduction and mitochondrial electron transport complex III is the predominant route of DQH2 oxidation. In the presence of cyanide, the addition of DQ also resulted in an increased rate of appearance of DQH2 and stimulation of cyanide-insensitive oxygen consumption. As DQH2 does not autoxidize-comproportionate over the study time course, these observations suggest a cyanide-stimulated one-electron DQ reduction and durosemiquinone (DQ*-) autoxidation. The latter processes are apparently confined to the cell interior, as the cell membrane impermeant oxidant, ferricyanide, did not inhibit the DQ-stimulated cyanide-insensitive oxygen consumption. Thus, regardless of whether DQ is reduced via a one- or two-electron reduction pathway, the net effect in the extracellular medium is the appearance of DQH2. These endothelial redox functions and their apposition to the vessel lumen are consistent with the pulmonary endothelium being an important site of DQ reduction to DQH2 observed in the lungs.

Topics: Animals; Benzoquinones; Cattle; Cells, Cultured; Endothelium, Vascular; Kinetics; Linoleic Acid; Models, Biological; Oxidation-Reduction; Pulmonary Artery

The interactions between duroquinol, linoleic acid, and lipoxygenase have been followed spectrophotometrically in the uv (210-340 nm) in a simple reaction medium (5 mM [4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid] buffer, pH 6.0). Duroquinol is oxidized by reacting with the peroxy radicals of linoleic acid generated in the presence of lipoxygenase. This oxidation is insensitive to cyanide but is sensitive to salicylhydroxamic acid, propylgallate, and disulfiram, the known inhibitors of lipoxygenase and of the cyanide-resistant electron transport pathway of plant mitochondria. This reaction is proposed as a model for the functioning of this pathway in plant mitochondria.

Topics: Benzoquinones; Cyanides; Electron Transport; Hydrogen-Ion Concentration; Hydroquinones; Linoleic Acid; Linoleic Acids; Lipoxygenase; Mitochondria; Oxidation-Reduction; Oxygen Consumption; Peroxides; Plants; Potassium Cyanide; Quinones; Spectrophotometry, Ultraviolet