BINDING OF ACETALDEHYDE TO RAT-LIVER MICROSOMES - ENHANCEMENT AFTER CHRONIC ALCOHOL-CONSUMPTION

Rat hepatic microsomal preparations were assessed for their capacity to bind exogenous 14C-acetaldehyde and 14C-adetaldehyde formed endogenously from 14C-ethanol in the microsomal ethanol-oxidizing system (MEOS). Exogenous acetaldehyde bound to rat liver microsomes. Blocking of the free amino groups and thiol groups with site specific reagents (pyridoxal 5''-phosphate and p-hydroxymercuribenzoate) reduced the binding of acetaldehyde. Acetaldehyde, formed endogenously from ethanol, also bound to hepatic microsomes. This was increased after chronic alcohol consumption, in association with enhanced MEOS activity. The binding of acetaldehyde produced by MEOS was significantly greater than that of an equivalent amount of exogenous acetaldehyde. Acetaldehyde produced in situ may exert local toxic effects on the endoplasmic reticulum.