RGD Reference Report - Leukocytes in carbon monoxide-mediated brain oxidative injury. - Rat Genome Database

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Leukocytes in carbon monoxide-mediated brain oxidative injury.

Authors: Thom, S R 
Citation: Thom SR, Toxicol Appl Pharmacol. 1993 Dec;123(2):234-47.
RGD ID: 13210748
Pubmed: PMID:8248931   (View Abstract at PubMed)
DOI: DOI:10.1006/taap.1993.1242   (Journal Full-text)

This study was conducted with rats to assess the involvement of leukocytes in a model of CO-mediated brain injury. Myeloperoxidase activity, measured as an index of leukocyte sequestration, was found to be increased 10-fold in brain microvessel segments prepared from rats immediately or 90 min after exposure to CO. Fluorescence and light microscopic examinations revealed leukocytes in microvessels taken from CO-poisoned rats, but not in that from control rats. Studies were then conducted with rats that had been made leukopenic or treated with monoclonal anti-CD-18 F(ab')2 fragments to inhibit leukocyte adherence to the vasculature. Neither of these groups of animals exhibited the biochemical changes observed in the brains of sham-treated rats: conversion of xanthine dehydrogenase (XD) to sulfhydryl-irreversible xanthine oxidase (XO), and lipid peroxidation, at 90 min following CO poisoning. Treatment with a synthetic serine protease inhibitor, gabexate mesylate, also prevented these biochemical changes if administered immediately after CO poisoning, but the agent did not inhibit leukocyte sequestration. Rats depleted of XD and XO by a tungsten diet, and those treated with allopurinol to inhibit XD and XO, also exhibited at least a 10-fold increase in myeloperoxidase activity in microvessels immediately after CO poisoning, but only a 5-fold increase at 90 min. In vitro studies demonstrated that B2 integrin-dependent polymorphonuclear leukocyte adherence was impaired immediately following CO poisoning although the adherence molecules were expressed on the membrane surface. Adherence function normalized by 45 min. The results suggest that leukocytes are responsible for the development of biochemical changes in brain following CO poisoning, and the sequence of events is as follows: leukocyte sequestration in the microvasculature, B2 integrin-dependent adherence, protease-mediated conversion of XD to XO, O2 radical-dependent lipid peroxidation.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Carbon Monoxide Poisoning  ISOXdh (Rattus norvegicus)13210748; 13210748 RGD 
Carbon Monoxide Poisoning  IEP 13210748 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to carbon monoxide  IEP 13210748 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Xdh  (xanthine dehydrogenase)

Genes (Mus musculus)
Xdh  (xanthine dehydrogenase)

Genes (Homo sapiens)
XDH  (xanthine dehydrogenase)


Additional Information