Free radical-mediated oxidative damage has been implicated in the path
ophysiological mechanisms of apoptosis. In this study we report that s
tatistically significant strand breaks were induced primarily in the h
ippocampus and cerebellum during chronic, and not acute, ethanol treat
ment. Damage to DNA observed in hippocampus and cerebellum was also co
rrelated with significant modification in the activities of mitochondr
ial respiratory complexes I and IV and with a significant increase in
lipid peroxidation products. This finding lends support to the fact th
at hippocampus and cerebellum are brain areas particularly vulnerable
to redox changes induced by alcohol intoxication, suggesting lower thr
eshold levels of ethanol tolerance.