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Tempol protection of spinal cord mitochondria from peroxynitrite-induced oxidative damage

Yiqin Xiong1, Indrapal N Singh, Edward D Hall

  • 1Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536, USA.

Free Radical Research
|June 11, 2009
PubMed

Insights

Peroxynitrite (PN) causes mitochondrial dysfunction after spinal cord injury (SCI) primarily through tyrosine nitration. The antioxidant tempol protects mitochondria by reducing this damage.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Mitochondrial Biology

Background:

  • Peroxynitrite (PN) is a reactive nitrogen species implicated in secondary injury following traumatic spinal cord injury (SCI).
  • Mitochondrial dysfunction is a key pathological event contributing to neuronal death after SCI.

Purpose of the Study:

  • To investigate the effects of the PN donor SIN-1 on isolated spinal cord mitochondria.
  • To evaluate the protective role of tempol, a PN scavenger, against SIN-1-induced mitochondrial damage.

Main Methods:

  • Isolated healthy spinal cord mitochondria were exposed to varying doses of SIN-1.
  • Mitochondrial respiration (respiratory control ratio, RCR) and protein modifications (3-nitrotyrosine, 4-hydroxynonenal) were assessed.
  • The effects of tempol on SIN-1-induced changes were evaluated.

Main Results:

  • SIN-1 exposure caused a dose-dependent decrease in RCR, indicating impaired mitochondrial respiration.
  • SIN-1 increased mitochondrial 3-nitrotyrosine levels, suggesting protein nitration, but not lipid peroxidation.
  • Tempol significantly protected mitochondrial function and reduced 3-nitrotyrosine levels.

Conclusions:

  • Exogenous PN rapidly induces mitochondrial oxidative damage and complex I dysfunction in spinal cord mitochondria, mimicking injury-induced changes.
  • Tyrosine nitration is the primary mechanism of PN-induced mitochondrial damage.
  • Tempol mitigates PN-induced mitochondrial dysfunction by reducing protein nitration.

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