Superoxide signaling in pain is independent of nitric oxide signaling

Hee Young Kim, Jigong Wang, Ying Lu, Jin Mo Chung, Kyungsoon Chung

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Two reactive oxygen species (ROS), nitric oxide (NO) and superoxide (O2), contribute to persistent pain. Using three different animal models where ROS mediate pain, this study examined whether NO and O2 converge to peroxynitrite (ONOO) or whether each has an independent signaling pathway to produce hyperalgesia. The hyperalgesia after spinal nerve ligation was attenuated by removing O2 by TEMPOL or inhibiting NO production by L-NAME, but not by removing peroxynitrite with FeTMPyP. Nitric oxide-induced hyperalgesia was not affected by removing O2 but was reduced by a guanyl cyclase inhibitor. Superoxide-induced hyperalgesia was not affected by inhibiting NO production but was suppressed by a protein kinase C inhibitor. The data suggest that NO and O2 operate independently to generate pain.

Original languageEnglish (US)
Pages (from-to)1424-1428
Number of pages5
Issue number16
StatePublished - Oct 28 2009
Externally publishedYes


  • Hyperalgesia
  • Pain signaling pathway
  • Peroxynitrite
  • Reactive oxygen species

ASJC Scopus subject areas

  • General Neuroscience


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