Oxidative damage induced by the injection of HIV-1 Tat protein in the rat striatum

Michael Y. Aksenov, Ulla Hasselrot, Arvind K. Bansal, Guanghan Wu, Avindra Nath, Carol Anderson, Charles F. MacTutus, Rosemarie M. Booze

Research output: Contribution to journalArticlepeer-review


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 languageEnglish (US)
Pages (from-to)5-8
Number of pages4
JournalNeuroscience Letters
Issue number1
StatePublished - Jun 1 2001
Externally publishedYes


  • HIV-related dementia
  • Oxidative stress
  • Tat

ASJC Scopus subject areas

  • Neuroscience(all)


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