Mitochondrial transport processes and oxidation of NADH by hypotonically-treated boar spermatozoa.
1. After hypotonic treatment spermatozoa have metabolic characteristics of mitochondria isolated from other cells. Ejaculated boar spermatozoa treated in this way can oxidise external NADH via both a lactate-pyruvate shuttle and a malate-aspartate cycle; this oxidation is coupled to the phosphorylation of ADP. 2. The dicarboxylate transport inhibitors butylmalonate, phenylsuccinate and bathophenanthroline sulphonate inhibit NADH oxidation dependent on added malate, glutamate and aspartate. alpha-Cyanocinnamate, a strong inhibitor of pyruvate transport, inhibits lactate-dependent NADH oxidation. 3. NADH oxidation dependent on malate, glutamate and aspartate is inhibited by uncoupling agents, but lactate-dependent NADH oxidation is stimulated. 4. Lactate-dependent NADH oxidation is inhibited by oxamate, an inhibitor of lactate dehydrogenase. Aminooxyacetate, an aminotransferase inhibitor, inhibits glutamate, malate and aspartate-dependent NADH oxidation. 5. Hypotonically-treated spermatozoa retain radioactivity after incubation with L-[U-14C]malate, [1,5-14C]citrate or [2-14C]malonate. Exchanges of retained radioactivity with various substrates indicate that dicarboxylate and tricarboxylate exchange carriers exist in the mitochondrial membrane.
D000818:Animals; D001692:Biological Transport; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D003998:Dicarboxylic Acids / Q000378:metabolism; D007038:Hypotonic Solutions; D007700:Kinetics; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009243:NAD / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010084:Oxidation-Reduction; D013094:Spermatozoa / Q000378:metabolism*; D013552:Swine
D003998:Dicarboxylic Acids; D007038:Hypotonic Solutions; D009840:Oligomycins; D009243:NAD; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone