Persistent pain is dependent on spinal mitochondrial antioxidant levels

Erica S. Schwartz, Young Kim Hee, Jigong Wang, Inhyung Lee, Eric Klann, Mo Chung Jin, Kyungsoon Chung

Research output: Contribution to journalArticlepeer-review


Reactive oxygen species (ROS) scavengers have been shown to relieve persistent pain; however, the mechanism is not clearly understood. Superoxide produced from mitochondrial oxidative phosphorylation is considered the major source of ROS in neurons during excitation where mitochondrial superoxide levels are normally controlled by superoxide dismutase (SOD-2). The present study hypothesizes that capsaicin-induced secondary hyperalgesia is a consequence of superoxide build-up in spinal dorsal horn neurons and SOD-2 is a major determinant. To test this hypothesis, the spinal levels of SOD-2 activity, inactivated SOD-2 proteins, and mitochondrial superoxide were measured and correlated to the levels of capsaicin-induced secondary hyperalgesia in mice with and without SOD-2 manipulations. The data suggest that superoxide accumulation is a culprit in the abnormal sensory processing in the spinal cord in capsaicin-induced secondary hyperalgesia. Our studies also support the notion that SOD-2 nitration is a critical mechanism that maintains elevated superoxide levels in the spinal cord after capsaicin treatment. Finally, our findings suggest a therapeutic potential for the manipulation of spinal SOD-2 activity in pain conditions.

Original languageEnglish (US)
Pages (from-to)159-168
Number of pages10
JournalJournal of Neuroscience
Issue number1
StatePublished - Jan 7 2009


  • Central sensitization
  • Mitochondria
  • Oxidative stress
  • Persistent pain
  • SOD-2
  • Superoxide

ASJC Scopus subject areas

  • General Neuroscience


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