Xanthine oxidase in experimental spinal cord injury.

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.

journal_name

J Neurotrauma

journal_title

Journal of neurotrauma

authors

Xu J,Beckman JS,Hogan EL,Hsu CY

doi

10.1089/neu.1991.8.11

subject

Has Abstract

pub_date

1991-04-01 00:00:00

pages

11-8

issue

1

eissn

0897-7151

issn

1557-9042

journal_volume

8

pub_type

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