Document Detail


Interaction of epicatechins derived from green tea with rat hepatic cytochrome P-450.
MedLine Citation:
PMID:  2894963     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Green tea has been used for generations in China and Asia as an antipyretic and diuretic. Prior studies have shown that extracts of green tea inhibit the mutagenicity of polycyclic aromatic hydrocarbons and aflatoxin B1. In this study, we investigated the interaction of certain flavonoid components of green tea epicatechin derivatives including (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin-3-gallate (ECG), and (-)-epigallocatechin-3-gallate (EGCG) with rat hepatic microsomal cytochrome P-450 (P-450). The addition of EC, EGC, ECG, and EGCG to hepatic microsomes prepared from phenobarbital (PB)-treated rats resulted in spectral changes characterized by absorbance maxima at 420 nm and minima at 380 nm, typical of modified Type II (reverse Type I) binding. Of the epicatechin derivatives, EGCG and ECG showed greater spectral change with oxidized P-450 and time- and concentration-dependent inhibition of the binding of carbon monoxide to dithionite-reduced cytochrome P-450. The addition of EC, EGC, ECG, and EGCG to microsomes prepared from control, PB- or 3-methylcholanthrene-treated rats resulted in a dose-dependent inhibition of cytochrome P-450-dependent aryl hydrocarbon hydroxylase, 7-ethoxycoumarin O-deethylase, and 7-ethoxyresorufin O-deethylase activities. EGCG was the most potent in this regard. Green tea polyphenols and epicatechin derivatives also significantly inhibited NADPH-cytochrome c reductase activity. An examination of the structure activity relationship of epicatechin derivatives suggests that the inhibitory effect on the microsomal enzyme system may be due to the galloyl groups or hydroxyl groups on the molecule. Our data indicate that these extracts of green tea may have potential as anticarcinogens.
Authors:
Z Y Wang; M Das; D R Bickers; H Mukhtar
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Drug metabolism and disposition: the biological fate of chemicals     Volume:  16     ISSN:  0090-9556     ISO Abbreviation:  Drug Metab. Dispos.     Publication Date:    1988 Jan-Feb
Date Detail:
Created Date:  1988-04-27     Completed Date:  1988-04-27     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9421550     Medline TA:  Drug Metab Dispos     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  98-103     Citation Subset:  IM    
Affiliation:
Department Dermatology, University Hospitals of Cleveland, Case Western Reserve University, Cleveland, OH.
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MeSH Terms
Descriptor/Qualifier:
Animals
Binding, Competitive
Carbon Monoxide / metabolism
Catechin / pharmacology*
Cytochrome P-450 Enzyme System / metabolism*
Epoxide Hydrolases / metabolism
Guanosine Triphosphate / metabolism
Liver / enzymology*
Male
Microsomes, Liver / metabolism
NADPH-Ferrihemoprotein Reductase / metabolism
Rats
Rats, Inbred Strains
Tea / analysis*
Grant Support
ID/Acronym/Agency:
AM34368/AM/NIADDK NIH HHS; CA-38028/CA/NCI NIH HHS; ES-1900/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Tea; 154-23-4/Catechin; 630-08-0/Carbon Monoxide; 86-01-1/Guanosine Triphosphate; 9035-51-2/Cytochrome P-450 Enzyme System; EC 1.6.2.4/NADPH-Ferrihemoprotein Reductase; EC 3.3.2.-/Epoxide Hydrolases

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


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