The metabolites and metabolic pathway of a new anticonvulsant drug, sodium dipropylacetate (DPA), in rat were investigated using
14C-labelled DPA. Most of the metabolites in urine and bile was glucronide and free DPA was as little as one-seventh of the total metabolites. In feces, only free DPA was detected, and the possibility of enterohepatic circulation of DPA was presumed. A part of dosed DPA was excreted in expired air in the form of CO
2. This degradative reaction took place in liver mitochondria and required CoA and oxygen. It was stimulated by ATP and EDTA, and inhibited by various enzymic reaction inhibitors such as malonate, Antimycin-A, chloropromazine, PCMB, and 2, 4-dinitrophenol. Therefore, this degradation is not a one-step reaction, decarboxylation, but must be β-oxidation of a fatty acid.
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