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Journal ArticleDOI

NADPH-dependent oxidation of methanol, ethanol, propanol and butanol by hepatic microsomes.

TLDR
Hematic microsomes catalyze the oxidation of methanol, ethanol, propanol and butanol to their respective aldehydes and appear responsible, at least in part, for the alcohol metabolism by the alcohol dehydrogenase independent pathway of the liver.
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This article is published in Biochemical and Biophysical Research Communications.The article was published on 1974-09-23. It has received 71 citations till now. The article focuses on the topics: Microsomal ethanol oxidizing system & Alcohol dehydrogenase.

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Citations
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Journal ArticleDOI

Microsomal ethanol-oxidizing system (MEOS): the first 30 years (1968-1998)--a review.

TL;DR: Enhanced ethanol oxidation is associated with cross-induction of the metabolism of other drugs, resulting in drug tolerance, and there is increased conversion of known hepatotoxic agents (such as CCl4) to toxic metabolites, which may explain the enhanced susceptibility of alcoholics to the adverse effects of industrial solvents.
Journal ArticleDOI

The discovery of the microsomal ethanol oxidizing system and its physiologic and pathologic role

TL;DR: Considering the pathogenic role that up‐regulation of CYP2E1 also plays in alcoholic liver disease, it is apparent that a major therapeutic challenge is now to find a way to control this toxic process.
Journal ArticleDOI

CYP2E1: from ASH to NASH.

TL;DR: No effective pharmacologic treatment is presently available but there is ongoing research on possible inhibitors of CYP2E1, innocuous enough to be suitable for chronic human consumption and sufficiently effective to attenuate the CYP1E1 induction to avoid the consequences of its excessive activity while maintaining its physiologic role.
Journal ArticleDOI

Induction of hepatic microsomal gamma-glutamyltransferase activity following chronic alcohol consumption.

TL;DR: It is suggested that increased serum gamma-glutamyltransferase activities commonly observed in alcoholism can be ascribed at least in part to an induction of microsomal gamma- GLUTamyl transferase activity.
Journal ArticleDOI

Hepatic microsomal alcohol-oxidizing system. Affinity for methanol, ethanol, propanol, and butanol.

TL;DR: It is suggested that the microsomal alcohol-oxidizing system accounts, at least in part, for that fraction of hepatic alcohol metabolism which is independent of the pathway involving alcohol dehydrogenase activity.
References
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Journal ArticleDOI

The colorimetric estimation of formaldehyde by means of the Hantzsch reaction

T. Nash
- 01 Oct 1953 - 
TL;DR: A chronology of key events leading up to and including the birth of Bonnichsen, R. K. & Bonner, J. (1952).
Journal Article

Pharmacological implications of microsomal enzyme induction

TL;DR: It is of considerable interest that certain inducers of liver microsomal enzymes have recently been used therapeutically for the treatment of hyperbilirubinemia in jaundiced children and for thetreatment of Cushing's syndrome.
Journal ArticleDOI

Hepatic Microsomal Ethanol-oxidizing System: IN VITRO CHARACTERISTICS AND ADAPTIVE PROPERTIES IN VIVO

TL;DR: The existence of a microsomal ethanol-oxidizing system, especially its capacity to increase in activity adaptively after ethanol feeding, may explain various effects of ethanol, including proliferation of hepatic smooth endoplasmic reticulum, induction of other hepaticmicrosomal drug-detoxifying enzymes, and the metabolic tolerance to ethanol which develops in alcoholics.
Journal ArticleDOI

Hepatic Microsomal Ethanol Oxidation

TL;DR: It is concluded that the NADPH-dependent microsomal ethanol-oxidizing system of Lieber and DeCarli is due to a hydrogen peroxide formation from NADPH and a subsequent peroxidation of ethanol by contaminating catalase.
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