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A malate‐oxaloacetate shuttle linking cytosolic fatty acid α‐oxidation to the mitochondrial electron transport chain in uncoupled fresh potato slices
Author(s) -
Wu Shuyi,
Laties George G.
Publication year - 1983
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.1983.tb04147.x
Subject(s) - biochemistry , malonate , rotenone , nad+ kinase , beta oxidation , mitochondrion , citric acid cycle , malate dehydrogenase , citrate synthase , electron transport chain , respiratory chain , biology , fatty acid , chemistry , metabolism , enzyme
The possible existence of a malonate‐sensitive dicarboxylate‐mediated electron shuttle between microsomal NAD‐linked fatty acid α‐oxidation and the mitochondrial electron transport chain in uncoupled fresh potato slices was investigated. Uncoupled slice respiration is inhibited by benzylmalonate and butylmalonate, inhibitors of dicarboxylate transport into mitochondria. Uncoupled slice respiration is also inhibited by rotenone, an indication of intramitochondrial NADH oxidation. Since fatty acid α‐oxidation per se is rotenone insensitive, rotenone and benzylmalonate inhibition of the oxidation of carboxyl‐labeled myristate in slices points to a dicarboxylic acid shuttle linking microsomal fatty acid a‐oxidation with intramitochondrial NADH dehydrogenase. Malonute inhibits both respiration and 14 CO 2 , release from carboxyl‐labeled myristate in fresh uncoupled slices, as do inhibitors of dicarboxylate transport. Mitochondrial studies show that malonate inhibits malate oxidation but not malate dehydrogenase per se. Furthermore, malonate inhibits malate transport more severely than malate oxidation. Accordingly, mulonate inhibition of uncoupled slice respiration in the absence of tricarboxylic acid cycle activity is attributed to its interference with mitochondrial malate transport, and its consequent curtailment of a putative malate‐OAA shuttle linked to cytosolic NAD‐mediated fatty acid α‐oxidation.