Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work studies some of the advances that have participated in the development of the liver transplantation-reperfusion injury. This lesion is a rather complex one that probably is not only associated with the production of free radicals, but also of other vasoactive substances such as, prostanoids, altered calcium related compounds, abnormal coagulation factors, as well as other important potentially harmful substances. Our interest since 1975, has resided in compounds that modify the xanthine oxidase pathway, such as allopurinol, that might either protect from the formation of free radicals or might act through other mechanisms such as, purine salvage and production of high energy compounds, among few of them. The pharmacological manipulation of the reperfusion injury, will require in this way, the use of various substances in the protection of the transplanted liver.
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PMID:Liver transplantation reperfusion injury. Factors in its development and avenues for treatment. 179 85

Hepatic transplantation may result in coagulopathy caused by the release of mast-cell-derived heparin, and xanthine oxidase (XO) inhibition stabilizes mast cells. Thus, XO inactivation could decrease coagulopathy after hepatoenteric ischemia-reperfusion. Rabbits were fed a standard or XO-inactivating diet before hepatoenteric ischemia for 35 min and before 30 min of reperfusion. Hemostasis was assessed by thrombelastography. Heparin activity was quantified by anti-IIa. XO inactivation resulted in clot formation after reperfusion in all animals, whereas only 37.5% of animals with XO activity clotted (P<0.05). Anti-IIa activity was less in animals at baseline and after reperfusion with XO inactivation (45+/-5 and 65+/-5 mU/mL, respectively) compared to animals with XO activity (51+/-4 and 71+/-5 mU/mL, respectively) (P<0.05). Clot strength, which was mediated by coagulation proteins, was significantly greater at baseline and after reperfusion in animals with XO inactivation. XO inactivation enhances hemostasis by decreasing circulating heparin activity and increasing coagulation protein function before ischemia-reperfusion.
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PMID:Coagulopathy mediated by hepatoenteric ischemia-reperfusion in rabbits: role of xanthine oxidase. 1243 67