Expression of Superoxide Dismutase Following Axotomy

doi:10.1006/exnr.1997.6604

Experimental Neurology

Volume 147, Issue 1, September 1997, Pages 37-47

https://doi.org/10.1006/exnr.1997.6604 Get rights and content

Abstract

Oxidative injury has been implicated in the pathophysiology of neuronal injury and neurodegenerative disease. Antioxidant proteins provide an endogenous defense against such oxidative injury and may yield important clues to mechanisms of cytoprotection and neuronal recovery. Axotomy is the simplest model of neuronal injury and lesioning the sciatic nerve allows concurrent study of both motor (spinal cord) and sensory (dorsal root ganglia, DRG) neurons affected by the same injury. This study was designed to examine the expression of superoxide dismutase (SOD), an essential antioxidant protein, in motor and sensory neurons following complete axotomy of peripheral nerve. Immunocytochemical, quantitative immunoblot, and enzymatic activity assay techniques are used. By 12 days after axotomy, immunocytochemical expression of Mn-SOD is markedly increased in affected DRG and spinal cord. A similar increase in Cu/Zn-SOD is not seen in DRG or spinal cord. This immunocytochemical staining is associated with a significant increase in specific activity and Mn-SOD protein content as measured on quantitative immunoblots. This report suggests, for the first time, that Mn-SOD and not Cu/Zn-SOD increases in sensory neurons of the DRG and motor neurons of the spinal cord following distal axotomy of the sciatic nerve. Quantitative measurements of Mn-SOD following axotomy reveals that the increase in immunocytochemical reactivity is associated with an approximately 30% increase in specific activity when comparing lesioned and contralateral spinal cord samples. These data suggest that Mn-SOD may have a more significant role in the pathophysiology of neuronal injury than Cu/ZnSOD.

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As the deprivation of trophic support caused by a nerve section is known to produce free radicals, it can be hypothesized that the modification of the redox status leads to an activation of a concomitant anti-oxidative stress response. The increase in Sod1 mRNA and its activity in DRG neurons after axotomy had already been demonstrated (Rosenfeld et al., 1997). Such a mobilization of antioxidant defenses might activate intracellular protective mechanism supporting neuronal survival.
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Regular ArticleExpression of Superoxide Dismutase Following Axotomy☆

Abstract

J. Biol. Chem.

Methods Enzymol.

Neuron

Exp. Neurol.

Lancet

Neurosci. Res.

J. Neurol. Sci.

Arch. Biochem. Biophys.