Evidence that infiltrating neutrophils do not release reactive oxygen species in the site of spinal cord injury

R. De Castro, M. G. Hughes, G. Y. Xu, C. Clifton, N. Y. Calingasan, Benjamin Gelman, D. J. McAdoo

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24 Scopus citations

Abstract

The release of reactive oxygen species (ROS) by neutrophils, which infiltrate the region of damage following spinal cord injury (SCI), was investigated to determine if such release is significant following spinal cord injury. The relationship of extracellular levels of hydroxyl radicals and hydrogen peroxide obtained by microdialysis sampling and oxidized protein levels in tissue to neutrophil infiltration following spinal cord injury was examined. Neither of the reactive oxygen species were elevated in the site of spinal cord injury relative to their concentrations in normal tissue at a time (24 h) when the numbers of neutrophils were maximum in the site of injury. Surprisingly, ablation with a neutrophil antiserum actually increased the level of oxidized proteins in Western blots. Thus, our findings are (1) that neutrophils, which infiltrate the site of damage following a spinal cord injury, do not release detectable quantities of reactive oxygen species; and (2) that the presence of neutrophils reduces the concentrations of oxidized proteins in the site of spinal cord injury. Therefore, release of reactive oxygen species by neutrophils does not contribute significantly to secondary damage following spinal cord injury. Reduced levels of oxidized proteins in the presence of neutrophils may reflect removal of damaged tissue by neutrophils.

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Keywords

  • Hydrogen peroxide
  • Hydroxyl radical
  • Microdialysis
  • Neutrophils
  • Protein oxidation
  • Secondary damage
  • Spinal cord injury

ASJC Scopus subject areas

  • Neurology
  • Neuroscience(all)

Cite this

Evidence that infiltrating neutrophils do not release reactive oxygen species in the site of spinal cord injury. / De Castro, R.; Hughes, M. G.; Xu, G. Y.; Clifton, C.; Calingasan, N. Y.; Gelman, Benjamin; McAdoo, D. J.

In: Experimental Neurology, Vol. 190, No. 2, 12.2004, p. 414-424.

Research output: Contribution to journalArticle