Abstract |
The induction of an experimental hepatitis did not affect the overall ability of the rat to metabolize the flavanol 3-O-(+)-[14C]methylcatechin by methylation or glucuronidation. The induction of hepatitis did cause a significant increase in metabolite excretion in urine (from 52% of the dose in control rats to 88% in hepatitis). Fecal excretion was correspondingly depressed (44 to 4% of the dose). In bile duct-cannulated rats, the induction of hepatitis prior to 3-O-(+)-[14C]methylcatechin administration resulted in low 14C excretion (38%) in bile (cf. 58% in bile of controls). The data obtained indicate that following induction of hepatitis biliary metabolites reabsorbed from the intestine are not reexcreted in bile in an enterohepatic cycle as in the normal rat but are excreted via the kidney. Induction of hepatitis did not affect the fast clearance of unchanged 3-O-methyl-(+)- catechin from plasma but plasma clearance of the metabolites was reduced from 112 to 89 ml/hr.
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Authors | A M Hackett, L A Griffiths |
Journal | Drug metabolism and disposition: the biological fate of chemicals
(Drug Metab Dispos)
1983 Nov-Dec
Vol. 11
Issue 6
Pg. 602-6
ISSN: 0090-9556 [Print] United States |
PMID | 6140147
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzopyrans
- meciadanol
- Galactosamine
- Catechin
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Topics |
- Animals
- Benzopyrans
(metabolism)
- Bile Ducts
(physiology)
- Catechin
(analogs & derivatives, metabolism)
- Galactosamine
- Hepatitis, Animal
(metabolism)
- Male
- Rats
- Rats, Inbred Strains
- Time Factors
- Tissue Distribution
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