ABSTRACT
This chapter reviews the evidence that Kupffer cells metabolize ethanol and discusses some theoretical mechanisms by which these cells may initiate or aggravate alcohol-induced hepatocyte damage. The capacity of all types of tissue macrophages, including Kupffer cells, to oxidize substantial quantities of ethanol to acetaldehyde and acetate and to release large amounts of acetaldehyde extracellularly is likely to be of considerable importance in the pathogenesis of ethanol-related tissue damage. One suggestion has been that the high concentrations of acetaldehyde generated at the surface of macrophages following ethanol consumption may react with and damage surrounding parenchymal cells. It is probable that little if any damage is caused by acetaldehyde generated and retained within normal hepatocytes as these cells rapidly oxidize intracellular acetaldehyde molecules and render them "nontoxic" via the action of acetaldehyde dehydrogenase. Acetaldehyde generated by Kupffer cells may also disturb the function of neighboring lipocytes.
