Journal of Lipid Research · 1965 · 66 citations · 7 references
PharmacyBiochemistryToxicologyAlcohol ToxicologyHepatotoxicologySubstance Abuse ToxicologyAlcohol MetabolismBlood Alcohol ConcentrationAcetaldehyde OxidationAcetaldehyde QuantificationBrain Ethanol ConcentrationBreath Alcohol Concentration MeasurementEthanol Concentration MeasurementHepatic Effects Of AlcoholHepatic Ketone Body ProductionLiver Toxicity Of Alcohol
A method for serial gas chromatographic determinations of acetaldehyde, acetone, and ethanol in alveolar air is described. The concentration of alcohol in alveolar air increased rapidly and then declined linearly following ingestion of ethanol, 0.5 ml/lb body weight, drunk as a 10% solution in 30 min. Acetaldehyde in alveolar air at first increased rapidly to a maximum concentration, then decreased only slightly for several hours despite rising or falling ethanol concentrations. The concentration of acetaldehyde then declined rapidly, beginning at the time when the ethanol concentration had returned to 15–25 μg/100 ml alveolar air.The concentrations of acetaldehyde in alveolar air appear to correspond to hepatic production. The plateau of acetaldehyde concentrations is probably due to the constant rate of ethanol oxidation over a wide range of ethanol concentrations.Intra-individual variations of replicate tests are small. Comparison of a group of five healthy control subjects with two alcoholics suffering from alcoholic brain damage showed elevated acetaldehyde curves in the latter group. Acetaldehyde concentrations were in the upper normal range in a jaundiced alcoholic suffering from hepatic cirrhosis. Elevated acetaldehyde concentrations may possibly be causally related to alcoholic brain damage.
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The metabolism of acetaldehyde by the brain <i>in vivo</i>
J. W. Ridge · Biochemical Journal · 1963 · 53 citations · Full text