Abstract
When pantethine was orally administered to rats at a clinical dose (10mg/ kg of body weight), the blood and liver acetaldehyde levels were significantly lower than those in untreated rats. On the contrary, the ethanol levels were not changed. The low acetaldehyde concentration following the ethanol might be due to an accelerated oxidation of acetaldehyde by activation of low-Km aldehyde dehydrogenase (ALDH), which was previously observed by pantethine-related metabolites formed in the liver.However, when pantethine was given intraperitoneally at a large dose (1.0g/ kg of body weight), elevation of blood and liver ethanol concentrations following ethanol loading to rats was rather inhibited. Ethanol absorption from the gastrointestinal tract might be decreased by pantethine-induced hypokinesia of the gastrointestine. When pantethine was administered intravenously (10mg/ kg of body weight) even at a clinical dose (20mg/ kg of body weight), acetaldehyde oxidation was severely inhibited. High acetaldehyde concentrations might be due to inhibition of low-Km ALDH by pantethine itself.
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