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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2004-6-17
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pubmed:abstractText |
Increased oxygen radical production may not only contribute to posttransplant ischemia-reperfusion injury but also to acute rejection of renal allografts. Xanthine oxidoreductase (XOR) may constitute a relevant reactive oxygen species (ROS) source. The study was conducted (1). to determine ROS production as well as oxidant and antioxidant enzyme activities in renal grafts and (2). to modulate acute rejection by tungsten administration, a specific inhibitor of XOR.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0041-1337
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
77
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1683-92
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15201667-Acute Disease,
pubmed-meshheading:15201667-Animals,
pubmed-meshheading:15201667-Catalase,
pubmed-meshheading:15201667-Graft Rejection,
pubmed-meshheading:15201667-Kidney,
pubmed-meshheading:15201667-Kidney Glomerulus,
pubmed-meshheading:15201667-Kidney Transplantation,
pubmed-meshheading:15201667-Kidney Tubules,
pubmed-meshheading:15201667-Multienzyme Complexes,
pubmed-meshheading:15201667-NADH, NADPH Oxidoreductases,
pubmed-meshheading:15201667-NADPH Oxidase,
pubmed-meshheading:15201667-Nephritis,
pubmed-meshheading:15201667-Oxidoreductases,
pubmed-meshheading:15201667-Postoperative Period,
pubmed-meshheading:15201667-Rats,
pubmed-meshheading:15201667-Rats, Inbred F344,
pubmed-meshheading:15201667-Rats, Inbred Lew,
pubmed-meshheading:15201667-Reactive Oxygen Species,
pubmed-meshheading:15201667-Transplantation, Homologous,
pubmed-meshheading:15201667-Transplantation, Isogeneic,
pubmed-meshheading:15201667-Tungsten,
pubmed-meshheading:15201667-Xanthine Dehydrogenase
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pubmed:year |
2004
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pubmed:articleTitle |
Role of xanthine oxidoreductase in experimental acute renal-allograft rejection.
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pubmed:affiliation |
Department of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
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pubmed:publicationType |
Journal Article
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