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Drug Metabolism & Disposition

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Abstract

Modulation of trans-4-acetylaminostilbene metabolism in the rat by methylcholanthrene and phenobarbital and its relevance for acute toxicity.

A Pfeifer and H G Neumann
Drug Metabolism and Disposition March 1988, 16 (2) 276-284;
A Pfeifer
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H G Neumann
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Abstract

trans-4-Acetylaminostilbene (trans-AAS) is acutely toxic to rats. Animals can be protected from the effects of a lethal dose by pretreatment with methylcholanthrene (MC), but not with phenobarbital (PB). In order to study the effects of these pretreatments on pharmacokinetic parameters, single, acute toxic doses of 3H-trans-AAS were orally administered to female Wistar rats and metabolism and excretion studied in untreated and PB- and MC-pretreated animals. MC pretreatment enhanced the rate of metabolism and the excretion of metabolites into the bile, but did not alter urinary excretion. After 3 days, 46, 86, and 52% of the administered dose was excreted, respectively, in untreated, MC-pretreated, and PB-pretreated animals. MC pretreatment modified both phase I and phase II metabolism of trans-AAS. Urinary excretion of unconjugated metabolites was decreased accompanied by an increased formation of sulfates. Biliary excretion of glucuronides and conjugated polar metabolites was increased by MC pretreatment. It is concluded that MC protects rats from acute trans-AAS toxicity by increasing the rate of total metabolism and enhancing metabolic (conjugation) pathways of inactivation relative to putative activation by oxidative metabolism.

 

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Drug Metabolism and Disposition
Vol. 16, Issue 2
1 Mar 1988
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Abstract

Modulation of trans-4-acetylaminostilbene metabolism in the rat by methylcholanthrene and phenobarbital and its relevance for acute toxicity.

A Pfeifer and H G Neumann
Drug Metabolism and Disposition March 1, 1988, 16 (2) 276-284;

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Abstract

Modulation of trans-4-acetylaminostilbene metabolism in the rat by methylcholanthrene and phenobarbital and its relevance for acute toxicity.

A Pfeifer and H G Neumann
Drug Metabolism and Disposition March 1, 1988, 16 (2) 276-284;
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