Document Detail


Evaluation of a screening method by liquid chromatography-tandem mass spectrometry for estimating effect of drugs on the activation and β-oxidation of fatty acids in mitochondria.
MedLine Citation:
PMID:  21054395     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Fatty acid metabolism is controlled not only by the acyl-coenzyme A (CoA) synthetases but by some enzymes in the β-oxidation cycle. Medium-chain and long-chain acyl-CoA esters are key metabolites in fatty acid metabolism. We have developed an enzymatic assay method for determining chain shortening of the acyl-CoAs via β-oxidation from palmitic and octanoic acids in liver mitochondria. We have evaluated the assay method for detecting whether drugs influence the activation or the β-oxidation of fatty acids.
METHODS: Liver mitochondria were used for investigating the effect of drugs on fatty acid metabolism. The drugs selected were salicylic acid, diclofenac, valproic acid and paracetamol. Each acyl-CoA formed was analysed by liquid chromatography-tandem mass spectrometry.
KEY FINDINGS: After less than 5 min of incubation, the levels of acyl-CoAs reflected the acyl-CoA synthetase activity, whereas after 60-min incubation they reflected the activity of some enzymes in the β-oxidation cycle. Salicylic acid, diclofenac and valproic acid inhibited the medium-chain acyl-CoA synthetases, whereas valproic acid only exhibited a weak inhibitory activity toward the β-oxidation of the medium-chain fatty acids. In the case of long-chain fatty acid metabolism, salicylic acid and diclofenac inhibited both the activation and β-oxidation, whereas valproic acid was a weak inhibitor for only the β-oxidation activity. Paracetamol showed hardly any influence on the metabolism of medium-chain and long-chain fatty acids.
CONCLUSIONS: These findings suggest that salicylic acid, diclofenac, valproic acid and paracetamol exert a different influence on fatty acid metabolism depending on the length of the acyl chain. This assay allows sensitive and selective analysis for predicting the pathways by which drugs exert a greater influence over fatty acid metabolism.
Authors:
Fumiyo Kasuya; Ryota Nishizawa; Teiichi Masuyama; Maya Kazumi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-04
Journal Detail:
Title:  The Journal of pharmacy and pharmacology     Volume:  62     ISSN:  2042-7158     ISO Abbreviation:  J. Pharm. Pharmacol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-08     Completed Date:  2011-05-11     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  0376363     Medline TA:  J Pharm Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1697-703     Citation Subset:  IM    
Copyright Information:
© 2010 The Authors. JPP © 2010 Royal Pharmaceutical Society of Great Britain.
Affiliation:
Biochemical Toxicology Laboratory, Faculty of Pharmaceutical Sciences, Kobegakuin University, Kobe, Japan. kasuya@pharm.kobegakuin.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Acetaminophen / pharmacology
Analgesics, Non-Narcotic / pharmacology
Animals
Anti-Infective Agents / pharmacology
Anti-Inflammatory Agents, Non-Steroidal / analysis,  pharmacology
Chromatography, Liquid / methods
Coenzyme A Ligases / antagonists & inhibitors,  metabolism
Diclofenac / metabolism,  pharmacology
Enzyme Inhibitors / pharmacology
Fatty Acids / antagonists & inhibitors,  metabolism*,  pharmacology
Lipid Metabolism / drug effects*
Male
Mice
Mice, Mutant Strains
Mitochondria, Liver / drug effects,  enzymology,  metabolism*
Oxidation-Reduction
Salicylic Acid / pharmacology
Tandem Mass Spectrometry / methods
Valproic Acid / pharmacology
Chemical
Reg. No./Substance:
0/Analgesics, Non-Narcotic; 0/Anti-Infective Agents; 0/Anti-Inflammatory Agents, Non-Steroidal; 0/Enzyme Inhibitors; 0/Fatty Acids; 103-90-2/Acetaminophen; 15307-86-5/Diclofenac; 69-72-7/Salicylic Acid; 99-66-1/Valproic Acid; EC 6.2.1.-/Coenzyme A Ligases

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


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