The Oxidative Response in the Chronic Constriction Injury Model of Neuropathic Pain

Tan, Edward C.T.H.; Bahrami, Soheyl; Kozlov, Andrey V.; Kurvers, Harry A.J.M.; Ter Laak, Henk J.; Nohl, Hans; Redl, Heinz; Goris, R. Jan. A.

doi:10.1016/j.jss.2008.03.035

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Volume 152, Issue 1 , Pages 84-88, March 2009

The Oxidative Response in the Chronic Constriction Injury Model of Neuropathic Pain

Edward C.T.H. Tan, M.D.
- Department of General Surgery, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
- To whom correspondence and reprint requests should be addressed at Radboud University Nijmegen Medical Centre, The Netherlands, 690 Department of General Surgery–Traumatology, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
Soheyl Bahrami, Ph.D.
- Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria
Andrey V. Kozlov, Ph.D.
- Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria
Harry A.J.M. Kurvers, M.D., Ph.D.
- Department of General Surgery, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
Henk J. Ter Laak, Ph.D.
- Departments of Pathology and Neurology, Radboud University Nijmegen Medical Centre, Nijemen, The Netherlands
Hans Nohl, Ph.D.
- Institute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria
Heinz Redl, Ph.D.
- Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria
R. Jan. A. Goris, M.D., Ph.D.
- Department of General Surgery, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Received 30 October 2007 published online 12 May 2008.

Background

In the chronic constriction injury model of rat neuropathic pain, oxidative stress as well as antioxidants superoxide dismutase and reduced glutathione (GSH) are important determinants of neuropathological and behavioral consequences. Studies of the chronic constriction injury model observed (indirect) signs of inflammation. We, therefore, investigated the level of oxidative stress and antioxidant enzymes in skeletal muscle tissue of the rat hind paw and (jugular vein) plasma at d 7 after nerve injury.

Materials and methods

The level of reactive oxygen and nitrogen species (RONS) was determined as a measure of oxidative stress. Reduced GSH levels and the ceruloplasmin/transferrin ratio were determined as measures of overall antioxidant activity. RONS and overall antioxidant activity were measured in skeletal muscle tissue of the hind paw and jugular vein plasma. The level of RONS in muscle was determined using spin trapping combined with electron paramagnetic resonance spectroscopy. Using electron paramagnetic resonance spectroscopy, we also determined plasma levels of transferrin and ceruloplasmin. GSH levels were determined using high-performance liquid chromatography.

Results

In skeletal muscle tissue, the level of RONS was lower in nerve-injured hind paws than in controls. The plasma level (jugular vein) of RONS did not differ between nerve-injured and control rats. In skeletal muscle tissue, the level of GSH was higher in nerve-injured hind paws than in controls. The ceruloplasmin/transferrin ratio tended to be higher in (jugular vein) plasma of nerve-injured rats as compared to controls.

Conclusions

This study shows that, at d 7 after nerve injury, oxidative stress-induced changes are present also in skeletal muscle tissue of the rat hind paw. Our findings of a decreased level of RONS in combination with an increased level of the antioxidant GSH suggest that an overshoot of antioxidant activity overrules initial oxidative stress.

Key Words: neuropathic animal model, oxygen free radicals, oxidative stress