Oxidative stress has been hypothesized to play a role in the pathogenesis o
f different neurodegenerative disorders, including HIV-related dementia. Ta
t, a nonstructural protein of HIV, is implicated in potentiation of neurona
l apoptosis by mechanisms involving the disruption of calcium homeostasis a
nd oxidative stress. The injection of Tar caused an increase of protein car
bonyl formation in the rat striatum. Increased oxidative modification of pr
oteins occurred early after Tat injection and preceded Tat-mediated astrogl
iosis. Immunostaining of brain sections demonstrated that an area of promin
ent protein carbonyl immunoreactivity surrounded an injection site in the s
triatum of Tat-injected rats. Intense protein carbonyl immunoreactivity was
localized in cell bodies. Our study suggests that increased protein oxidat
ion may be an important part of the mechanism of Tat neurotoxicity. (C) 200
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