The influence of acute ethanol administration on the oxidative stress
status of rat brain and liver was assessed by in situ spontaneous orga
n chemiluminescence (CL). Brain and liver CL was significantly increas
ed after acute ethanol administration to fed rats, a response that is
time-dependent and evidenced at doses higher than 1 g/kg. Ethanol-indu
ced CL development is faster in liver compared with brain probably due
to the greater ethanol metabolic capacity of the liver, whereas the n
et enhancement in brain light emission at 3 h after ethanol treatment
is higher than that of the liver, which could reflect the greater susc
eptibility of brain to oxidative stress. The effect of ethanol on brai
n and liver CL seems to be mediated by acetaldehyde, due to its abolis
hment by the alcohol dehydrogenase inhibitor 4-methylpyrazole and exac
erbation by the aldehyde dehydrogenase inhibitor disulfiram. In brain,
these findings were observed in the absence of changes in the activit
y of superoxide dismutase, catalase, glutathione peroxidase, glutathio
ne reductase, and glucose-6-phosphate dehydrogenase. However, the cont
ent of brain glutathione was significantly decreased by 31% by ethanol
, thus establishing an enhanced oxidative stress in this tissue. (C) 1
997 Elsevier Science Ireland Ltd.