Document Detail


Human CYP2C9 and CYP2A6 mediate formation of the hepatotoxin 4-ene-valproic acid.
MedLine Citation:
PMID:  9353388     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cytochrome P450-dependent desaturation of the anticonvulsant drug valproic acid (VPA) results in formation of the hepatotoxin, 4-ene-VPA. Polytherapy with other anticonvulsants which are known P450 inducers increases the flux through this bioactivation pathway. The aim of the present study was to identify specific, inducible forms of human liver P450 which catalyze terminal desaturation of VPA. Oxidized VPA metabolites formed in an NADPH-dependent manner by human liver microsomes were quantified by gas-chromatography/mass spectrometry. In vitro reaction conditions were established which reflected the product profile found in vivo. Production of 4-ene-VPA by microsomal P450s could be inhibited significantly by coumarin, sulfaphenazole and diethyldithiocarbamate, but not by triacetyloleandomycin, quinidine or furafylline. Recombinant human CYP3A4 did not form detectable levels of 4-ene-VPA and, of nine additional isoforms expressed in either HepG2 or lymphoblastoid cells which were screened for VPA desaturase activity, only CYP2C9 and CYP2A6 formed detectable levels of metabolite. Consequently, CYP3A4, the isoform usually associated with induction by anticonvulsants cannot be responsible for the enhanced 4-ene-VPA formation that occurs during polytherapy. Instead, enhanced activity in vivo likely results from induction of CYP2A6 and/or CYP2C9.
Authors:
A J Sadeque; M B Fisher; K R Korzekwa; F J Gonzalez; A E Rettie
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  283     ISSN:  0022-3565     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  1997 Nov 
Date Detail:
Created Date:  1997-12-08     Completed Date:  1997-12-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  698-703     Citation Subset:  IM    
Affiliation:
Department of Medicinal Chemistry, University of Washington, Seattle, Washington 98195, USA.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Anticonvulsants / metabolism*
Aryl Hydrocarbon Hydroxylases*
Child
Cytochrome P-450 Enzyme System / physiology*
Fatty Acids, Monounsaturated / metabolism*,  toxicity
Female
Humans
Liver / drug effects*,  metabolism
Male
Middle Aged
Mixed Function Oxygenases / physiology*
Steroid 16-alpha-Hydroxylase*
Steroid Hydroxylases / physiology*
Valproic Acid / metabolism*
Grant Support
ID/Acronym/Agency:
GM07750/GM/NIGMS NIH HHS; GM32165/GM/NIGMS NIH HHS; GM49054/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Anticonvulsants; 0/Fatty Acids, Monounsaturated; 1575-72-0/2-propyl-4-pentenoic acid; 9035-51-2/Cytochrome P-450 Enzyme System; 99-66-1/Valproic Acid; EC 1.-/Mixed Function Oxygenases; EC 1.14.-/Steroid Hydroxylases; EC 1.14.14.1/Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1/CYP2C9 protein, human; EC 1.14.14.1/Steroid 16-alpha-Hydroxylase; EC 1.14.14.1/coumarin 7-hydroxylase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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