Oxidative phosphorylation in rat oral mucosal mitochondria.
Oral mucosal mitochondria were isolated and characterized morphologically by electron microscopy. Polarographic measurements were made of respiration and oxidative phosphorylation in the mitochondrial preparations. ADP:O ratios approaching or slightly exceeding the theoretical maxima and stabilized respiratory control ratios were achieved with malate + glutamate, succinate and ascorbate-N,N,N1N1 tetramethyl-p-phenylenediamine (TMPD) as substrates. Inhibition by rotenone, antimycin A, azide, and cyanide established the classical electron transport chain as the major pathway of mitochondrial respiration. Respiration of the oral mucosal mitochondria was stimulated by DNP in the presence of succinate. DNP-stimulated respiration exceeded that observed in the presence of ADP plus Pi and increasing the concentration of DNP progressively inhibited respiration.
D000135:Acid Phosphatase / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D004140:Dinitrophenols / Q000494:pharmacology; D004579:Electron Transport; D003576:Electron Transport Complex IV / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D009061:Mouth Mucosa / Q000378:metabolism* / Q000648:ultrastructure; D009251:NADPH-Ferrihemoprotein Reductase / Q000378:metabolism; D009708:Nucleotidases / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D012402:Rotenone / Q000494:pharmacology; D014503:Urate Oxidase / Q000378:metabolism
D004140:Dinitrophenols; D012402:Rotenone; D000255:Adenosine Triphosphate; D009251:NADPH-Ferrihemoprotein Reductase; D014503:Urate Oxidase; D003576:Electron Transport Complex IV; D009708:Nucleotidases; D000135:Acid Phosphatase