Abstract
Summary Rat hepatic microsomal preparations were assessed for their capacity to bind exogenous 14C-acetaldehyde and 14C-acetaldehyde formed endogenously from 14C-ethanol in the microsomal ethanol-oxidizing system (MEOS). Exogenous acetaldehyde was found to bind 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. Thus, acetaldehyde produced in situ may exert local toxic effects on the endoplasmic reticulum.
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