Determination of hepatic acetaldehyde and its biphasic relationship to the ethanol concentration in rats.

Abstract

In situ freeze clamping of livers using either pentobarbital anaesthesia (40 mg/kg) or cervical dislocation as means of sacrificing rats were compared in regard to the determination of the hepatic acetaldehyde (AcH) concentration following ethanol exposure. It was demonstrated that following cervical dislocation, the AcH concentration decreased by 50%, ethanol decreased by 7%, and the mitochondrial redox state, expressed by the 3-hydroxybutyrate/acetoacetate ratio, increased by 100% within 40 s. The extrapolated 0-time values for AcH, ethanol concentration, and 3-hydroxybutyrate/acetoacetate ratio were equal to values obtained from pentobarbital anaesthetized rats. AcH concentrations (5 to 100 microM) were also measured 60 minutes after administration of increasing doses of ethanol. A positive correlation between the hepatic AcH and ethanol concentration was found up to ethanol concentrations of about 20 mM, suggesting either an increase in ethanol oxidation, a decrease in AcH oxidation, or both were present concomitant with increasing ethanol concentrations. When ethanol concentrations were above 20 mM, a negative correlation between AcH level and ethanol concentration was observed, suggesting a decrease in ethanol oxidation, an increase in AcH oxidation, or both were occurring.