Hyperoxia increases AP-1 DNA binding in rat brain

Li Qi Tong, Tracy Toliver-Kinsky, David Rassin, Karin Werrbach-Perez, Jose R Perez-Polo

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Oxidative stress appears to contribute to neurodegenerative outcomes after ischemia, hypoxia, and hyperoxia. The AP-1 transcription factor is made up of a family of regulatory proteins that can be activated by oxidative stress. In the present study, we examined AP-1 DNA binding activity in terms of specific participating AP-1 proteins in rat brain after hyperoxia. Male Sprague-Dawley rats were exposed to 100% oxygen under isobaric conditions over time. The AP-1 DNA binding activity present in the rat hippocampus and basal forebrain was characterized by electrophoretic mobility shift analysis (EMSA) and the participating AP-1 proteins identified by immunodepletion/supershift and Western blotting analyses. The Fos and Jun proteins were localized by immunohistochemistry to hippocampus. There were significant increases in AP-1 DNA binding in both hippocampus and basal forebrain after hyperoxia. There was also a significant increase in c-Jun protein levels and the proportion of c-Jun present in AP-1 DNA binding complexes in hippocampal nuclei after hyperoxia. These results suggest that AP-1 activation via c-Jun binding to DNA is an important component of brain responses to oxidative stress.

Original languageEnglish (US)
Pages (from-to)111-115
Number of pages5
JournalNeurochemical Research
Issue number1
StatePublished - Jan 1 2003
Externally publishedYes


  • AP-I
  • Basal forebrain
  • Hippocampus
  • Hyperoxia
  • Oxidative stress
  • c-Jun

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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