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Lowering of Blood Acetaldehyde but Not Ethanol Concentrations by Pantethine following Alcohol Ingestion: Different Effects in Flushing and Nonflushing Subjects
Author(s) -
Watanabe Akiharu,
Hobara Norio,
Kobayashi Michio,
Nakatsukasa Harushige,
Nagashima Hideo
Publication year - 1985
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1985.tb05748.x
Subject(s) - acetaldehyde , aldehyde dehydrogenase , chemistry , ethanol , ingestion , alcohol , alcohol dehydrogenase , taurine , ethanol metabolism , endocrinology , medicine , biochemistry , pharmacology , enzyme , amino acid
A rise in Mood acetaldehyde concentration* foftowmg alcohol ingestion was significantly inhibited when healthy nonflushing sutojecti were administered a clinical dose of pantethine oraty. However, similar findings were not observed in flushing (alcohol‐sensitive) subjects lacking hepatic low K m aldehyde dehydrogenase (ALOH). The blood ethanol concentrations were not altered by this treatment in either flushing or nonflushing subjects. Acetaldehyde (45 μM) added in vitro to whole blood and plasma obtained 1 hr after pantethine administration disappeared as the incubation continued similarly as with blood and plasma obtained prior to pantethine treatment Pantethine‐related metabolites, such as taurine, pantetheine, coenzyme A, and pantothenate, activated ALOH in vitro. Hepatic acetaldehyde levels following ethanol loading of rats treated with pantethine were much lower than in untreated rats. The pantethine action observed only in nonflushing subjects might be due to an accelerated oxidation of acetaldehyde by the activation of low K m ALOH by pantethine‐related metabolites formed in the liver.