The inhibition by valproic acid of the mitochondrial oxidation of monocarboxylic and omega-hydroxymonocarboxylic acids: possible implications for the metabolism of gamma-aminobutyric acid.
The inhibition by valproic acid of the mitochondrial oxidation of monocarboxylic and omega-hydroxymonocarboxylic acids: possible implications for the metabolism of gamma-aminobutyric acid.
复制标题
丙戊酸对单羧酸和 omega-羟基单羧酸线粒体氧化的抑制:对 γ-氨基丁酸代谢的可能影响。
DOI:
10.1093/oxfordjournals.jbchem.a122036
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发表时间:
1987
影响因子:
2.7
通讯作者:
Vamecq,J
中科院分区:
文献类型:
--
作者:
Draye,JP;Vamecq,J
MATERIALS AND METHODSMaterials-Homovanillic acid and peroxidase Type II were purchased from Sigma Chemical Co.(St. Louis, Mo., USA). FAD, CoA, NAD, ADP, and ATP were from Boehringer Pharma (Mannheim, BRD). CoA and carnitine deriva tives of palmitic, lauric, and butyric acids were obtained from Pharmacia (Uppsala, Sweden). Valproic, palmitic, lauric, decanoic, octanoic, butyric, 16-hydroxypalmitic, 12-hydroxylauric, and 4-hydroxybutyric acids were from Janssen Chemica (Beerse, Belgium) and 10-hydroxydecanoic acid from Aldrich Chemie (Brussels, Belgium). Potas sium ferricyanide was purchased from Merck (Darmstadt, BRD).Animals-Adult male albino Wistar rats (200-300 g) were fed on a standard laboratory animal chow. Valproate-treated animals were fed on a solid diet made by mixing the powdered animal chow with either 0.5 or 0.1%(w/w) neutralized valproic acid. Clofibrate-treated rats received a 0.5%(w/w) clofibrate-containing diet.