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Palmitoyl‐CoA Elongation in Brain Microsomes: Dependence on Cytochrome b 5 and NADH‐Cytochrome b 5 Reductase
Author(s) -
Takeshita Masazumi,
Tamura Minoru,
Yoshida Satoshi,
Yubisui Toshitsugu
Publication year - 1985
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1985.tb07204.x
Subject(s) - reductase , cytochrome , biochemistry , microsome , cytochrome p450 reductase , cytochrome c , electron transport chain , malonyl coa , cytochrome b , fatty acid , coenzyme q – cytochrome c reductase , biology , enzyme , chemistry , mitochondrion , beta oxidation , mitochondrial dna , gene
Experiments were performed to demonstrate the involvement of electron transport system in fatty acid elongation in rat brain microsomes. Mercuric chloride and p ‐chloromercuriphenylsulfonate, inhibitors on NADH‐cytochrome b 5 reductase, at 32 μ M inhibited NADH‐supported palmitoyl‐CoA elongation to 30 and 60% of control activity, respectively, whereas NADPH‐supported palmitoyl‐CoA elongation was unaffected by these mercurials. An antibody to rat liver NADH‐cytochrome b 5 reductase inhibited brain microsomal NADH‐cytochrome b 5 reductase activity and NADH‐dependent palmitoyl‐CoA elongation. Treatment of brain microsomes with trypsin diminished the cytochrome b 5 content; NADH‐ and NADPH‐cytochrome c reductase activities were significantly decreased, but the decrease in NADH‐cytochrome b 5 reductase activity was relatively small. Whereas essentially no incorporation of malonyl‐CoA into palmitoyl‐CoA was observed with trypsintreated microsomes, addition of detergent‐solubilized cytochrome b 5 resulted in a recovery of fatty acid elongation. These results indicate the presence of an electron transport system, NADH‐NADH‐cytochrome b 5 reductase–cytochrome b 5 ‐fatty acid elongation, in brain microsomes.