Study and objectives: (Na + K)-adenosine
triphosphatase (ATPase) activity, oxidative stress parameters, and
morphologic characteristics of the lung and kidney of rats under acute
ethanol intoxication were assessed to investigate the pathogenic
mechanism of tissue damage.
Design and interventions:
Adult rats were given ethanol (5.5 g/kg) 3 h before performing the
biochemical and morphologic studies. Oxidative stress was assessed by
measuring the levels of reduced glutathione (GSH) and glutathione
disulfide (GSSG), the activities of key antioxidant enzymes
(ie, catalase [CAT], superoxide dismutase [SOD], and
glutathione peroxidase [GSH-Px]) and malondialdehyde production.
(Na + K)-ATPase, a membrane-bound enzyme, also was assayed.
Results: In the lung, ethanol increased MDA production by
60%, decreased GSH levels by 33%, decreased SOD and GSH-Px activity
by 10%, and decreased (Na + K)-ATPase activity by 55%, whereas CAT
activity was unaltered. Impaired surfactant secretion and cell
adhesion of lung epithelial cells were found. In the kidney, ethanol
did not influence the activity of (Na + K)-ATPase or lipid
peroxidation, despite the reduction of both GSH and the GSH/GSSG ratio.
Focally thickened glomerular basement membrane, apoptosis of foot
processes, and tubulointerstitial fibrosis were found.
Conclusions: These data suggest that oxidative stress plays
a role in mediating the ethanol-induced down-regulation of lung
(Na + K)-ATPase. GSH depletion seems to be a major determinant of
this effect. Independent mechanisms seem to account for the morphologic
alterations of these organs.