Characterization of brain acetaldehyde oxidizing systems in the mouse.

C57BL mice were treated (75 or 100 mg/kg) with pargyline or Lilly 51641 90 min prior to sacrifice. Liver and brain subcellular fractionation revealed that pretreatment with these drugs resulted in a significant inhibition of aldehyde dehydrogenase (ALDH) in liver cytosol and mitochondria, while brain ALDH in these same fractions was unaffected. Administration of pargyline or Lilly 51641 prior to ethanol treatment (3.0 g/kg) resulted in a significant elevation of blood acetaldehyde. Significant increases in brain acetaldehyde concentrations were not observed until blood acetaldehyde levels surpassed 200 nmol/ml. When mice were injected with ethanol (3.0 g/kg) and acetaldehyde (200 mg/kg), a similar relationship between blood and brain acetaldehyde concentrations was observed. Data presented in the present study indicate that there are very efficient enzymatic mechanisms responsible for acetaldehyde oxidation in brain and that at blood acetaldehyde concentratins normally occurring after ethanol ingestion, brain acetaldehyde levels would be extremely low.