Abstract
Oxidative stress has been hypothesized to play a role in the pathogenesis of different neurodegenerative disorders, including HIV-related dementia. Tat, a nonstructural protein of HIV, is implicated in potentiation of neuronal apoptosis by mechanisms involving the disruption of calcium homeostasis and oxidative stress. The injection of Tat caused an increase of protein carbonyl formation in the rat striatum. Increased oxidative modification of proteins occurred early after Tat injection and preceded Tat-mediated astrogliosis. Immunostaining of brain sections demonstrated that an area of prominent protein carbonyl immunoreactivity surrounded an injection site in the striatum of Tat-injected rats. Intense protein carbonyl immunoreactivity was localized in cell bodies. Our study suggests that increased protein oxidation may be an important part of the mechanism of Tat neurotoxicity.
Original language | English (US) |
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Pages (from-to) | 5-8 |
Number of pages | 4 |
Journal | Neuroscience Letters |
Volume | 305 |
Issue number | 1 |
DOIs | |
State | Published - Jun 1 2001 |
Externally published | Yes |
Keywords
- HIV-related dementia
- Oxidative stress
- Tat
ASJC Scopus subject areas
- General Neuroscience