Selenium is an important factor as a component of glutathione peroxidase. In circumstances like chronic alcoholism, involving increased activity of free radicals, selenium deficiency can augment tissue degeneration by enhancing lipid peroxidation. In the present study, selenium was given to rats fed an alcohol-rich diet and the extent of liver injury was assessed by measuring prolidase I activity as well as hydroxyproline and free proline levels in the liver tissue after five months of ethanol ingestion. These findings were compared with the levels in controls and in the rats receiving sodium selenite in addition to ethanol. Hepatic prolidase activity increased in both groups receiving alcohol. There was no change in tissue hydroxyproline levels. We conclude that tissue (or serum) prolidase I activity may be useful for the early detection of alcoholic liver injury or other forms of oxidant-induced liver damage.