Free radical generation is hypothesized to be the cause of alcohol-ind
uced tissue injury. Using fluorescent cis-parinaric acid and TEARS, li
pid peroxidation was shown to be increased in the presence of trace am
ounts of free ferrous ion in PC12 cells. This increase in lipid peroxi
dation was enhanced by ethanol in a dose dependent manner and also cor
related with loss of cell viability, as measured by increased release
of lactate dehydrogenase (LDH). Resveratrol, a potent antioxidant, had
a protective effect against lipid peroxidation and cell death. These
findings strongly suggest that ethanol-induced tissue injury end cell
death is a free radical mediated process, and may be important in alco
hol-related premature aging and other degenerative diseases.