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Xanthine oxidase in experimental spinal cord injury.
J Neurotrauma. 1991 Spring; 8(1):11-8.JN

Abstract

The excessive generation of free radicals is thought to be one of the major mechanisms leading to tissue injury in various pathological conditions, including ischemia, inflammation, and trauma. Conversion of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) contributes to the formation of superoxide, an oxygen radical. We measured XDH and XO activity using a newly developed fluorometric assay in an experimental spinal cord injury model in rats. XO activity increased by more than 100% 4 h after spinal cord trauma. Total (XDH + XO) activity also increased by 96% during the same period. Allopurinol, an inhibitor of XO (100 mg/kg/day x 2 days, i.p.), completely inhibited plasma and spinal cord XO activity but did not affect posttraumatic edema determined by water content or polymorphonuclear (PMN) cell infiltration reflected by myeloperoxidase (MPO) activity in traumatized spinal cord. These results indicate that XDH conversion to XO may not be the major mechanism of oxygen radical formation in the pathogenesis of vasogenic edema or inflammatory response in this experimental spinal cord injury model in rats.

Authors+Show Affiliations

Department of Neurology, Medical University of South Carolina, Charleston.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1649310

Citation

Xu, J, et al. "Xanthine Oxidase in Experimental Spinal Cord Injury." Journal of Neurotrauma, vol. 8, no. 1, 1991, pp. 11-8.
Xu J, Beckman JS, Hogan EL, et al. Xanthine oxidase in experimental spinal cord injury. J Neurotrauma. 1991;8(1):11-8.
Xu, J., Beckman, J. S., Hogan, E. L., & Hsu, C. Y. (1991). Xanthine oxidase in experimental spinal cord injury. Journal of Neurotrauma, 8(1), 11-8.
Xu J, et al. Xanthine Oxidase in Experimental Spinal Cord Injury. J Neurotrauma. 1991;8(1):11-8. PubMed PMID: 1649310.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Xanthine oxidase in experimental spinal cord injury. AU - Xu,J, AU - Beckman,J S, AU - Hogan,E L, AU - Hsu,C Y, PY - 1991/1/1/pubmed PY - 1991/1/1/medline PY - 1991/1/1/entrez SP - 11 EP - 8 JF - Journal of neurotrauma JO - J Neurotrauma VL - 8 IS - 1 N2 - The excessive generation of free radicals is thought to be one of the major mechanisms leading to tissue injury in various pathological conditions, including ischemia, inflammation, and trauma. Conversion of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) contributes to the formation of superoxide, an oxygen radical. We measured XDH and XO activity using a newly developed fluorometric assay in an experimental spinal cord injury model in rats. XO activity increased by more than 100% 4 h after spinal cord trauma. Total (XDH + XO) activity also increased by 96% during the same period. Allopurinol, an inhibitor of XO (100 mg/kg/day x 2 days, i.p.), completely inhibited plasma and spinal cord XO activity but did not affect posttraumatic edema determined by water content or polymorphonuclear (PMN) cell infiltration reflected by myeloperoxidase (MPO) activity in traumatized spinal cord. These results indicate that XDH conversion to XO may not be the major mechanism of oxygen radical formation in the pathogenesis of vasogenic edema or inflammatory response in this experimental spinal cord injury model in rats. SN - 0897-7151 UR - https://www.unboundmedicine.com/medline/citation/1649310/Xanthine_oxidase_in_experimental_spinal_cord_injury_ L2 - https://www.liebertpub.com/doi/10.1089/neu.1991.8.11?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -