We studied the role of free radicals on brain oxidative damage in rats afte
r acute immobilization stress (restraint) and mild emotional stress (handli
ng). To investigate brain oxidative damage, CuZn and Mn dependent superoxid
e dismutase (CuZn SOD, Mn SOD) activities, lipid peroxidation (TBARs), Na+K
+ ATPase activity, protein carbonyl (PrC), and reduced and oxidized glutath
ione (GSH GSSG) levels were measured in the cerebral cortex (CTX), hippocam
pus (HIP), and striatum (ST) of the animals after the two different stress
stimuli. Because stress produces abnormalities in the hypothalamic-p pituit
ary-adrenal axis, the intensity of the two stress conditions were measured
by plasmatic corticosteroid (COR) levels: particularly, COR levels doubled
in handled rats and increased 15-fold in restrained animals. The SOD activi
ties increased in CTX and decreased in HIP of the handled rats, while in ST
a significant decrease in handled animals but an increase in restrained an
imals occurred. TBARs, GSH, and GSSG levels remained unchanged while an ind
ex of glutathione redox decreased significantly in ST of handled animals an
d in CTX of restrained ones. Na+K+ ATPase activity increased significantly
in the HIP and ST of both groups of stressed rats. The stress induced a rem
arkable increase in PrC levels in all studied cerebral areas. These finding
s provide evidence to support the idea that stress produces oxidants but th
at the oxidative damage in stress differs in cerebral areas and could contr
ibute to the degenerative mechanism of aging.