Contribution of exogenous ethanol and endogenous substrates to acetaldehyde-adduct formation in liver injury.

Acetaldehyde was found to be transported in the blood mainly bound reversibly to 2 components of the red blood cells (RBC): a) hemoglobin, which provides binding of a high affinity, but low capacity, and b) a non-protein component (presumably cysteine), which has a lower affinity but a higher capacity. In alcoholics, the main increase in RBC-acetaldehyde binding occurred in the protein-free fraction, in association with a marked increase in RBC-cysteine. Elevated RBC-acetaldehyde persisted for at least 2 weeks after alcohol withdrawal in 83% of the blood samples from alcoholics. Even in the absence of alcohol consumption, liver injury increased acetaldehyde from sources other than ethanol. This was associated with high serum antibody titers against acetaldehyde adducts. In an animal model of non-alcoholic liver cirrhosis, a target protein for the formation of acetaldehyde adducts appears to be procollagen type I.