Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.17.1.4 (xanthine dehydrogenase)
 1,236 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Xanthine oxidase (XO)-derived oxygen radicals are thought to play an important role in the intestinal injury resulting from ischemia and reperfusion. In vitro data shows enhanced XO activity in the presence of histamine. Histamine is known to be released during intestinal ischemia and reperfusion. The purpose of this study was to evaluate the relationship between histamine and XO in vivo in intestinal ischemia/reperfusion injury. Using an established model of gut ischemia and reperfusion, portal venous plasma was obtained and assayed for histamine levels, XO activity, and xanthine dehydrogenase (XD) activity following injury. Intestinal ischemia for 120 minutes resulted in a 200% increase in plasma histamine levels (263.4 +/- 36.9 nmol/mL control, v 548.7 +/- 35.1 nmol/mL experimental, P less than .05). Reperfusion for 15 minutes resulted in a further increase in plasma histamine (to 658.3 +/- 33.9 nmol/mL), compared with 120 minutes of ischemia alone. No significant change in plasma XO activity resulted after simple ischemia for 120 minutes. However, XO activity doubled within 15 minutes of reperfusion of the ischemic intestine (6.37 +/- 0.53 nmol O2- per milliliter per minute v 3.12 +/- 0.25 nmol O2- per milliliter per minute, P less than .05). Reperfusion for 60 minutes resulted in the maximal observed increase in plasma XO activity (9.49 +/- 0.67 nmol O2- per milliliter per minute). Analysis of XD activity demonstrated no significant decrease compared with controls until 120 minutes of ischemia and 60 minutes of reperfusion (1.62 +/- 0.49 nmol uric acid per milliliter per minute at 60 minutes of reperfusion, versus 5.02 +/- 0.52 nmol uric acid per milliliter per minute control, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histamine: a promoter of xanthine oxidase activity in intestinal ischemia/reperfusion. 168 83

Intestinal ischemia, however, caused, is still a serious and growing clinical problem with an unacceptable mortality rate of over 60%. This high mortality rate is mainly due to the fact that the patients are not admitted to the hospital or not treated early enough. Even if the patients are operated on within 24 h, their mortality rate is still over 50%, and those surviving the initial treatment suffer from postischemic complications. These damages have been accounted until now to tissue ischemia. It has been proven experimentally that also reperfusion or revascularization after time-limited ischemia add to the tissue damages observed, due to the formation of O2-radicals. Thereby the prerequisites for the production of these radicals (the conversion of xanthine dehydrogenase to xanthine oxidase and the increase of hypoxanthine concentrations in the tissue and plasma) are generated during tissue ischemia. These radicals damage directly or initiate several vicious circles leading to mucosal lesions, impaired intestinal function and an enhanced absorption of bacteria and endotoxin. Various substances (SOD, catalase, DMSO, allopurinol, deferoxamine etc.) detoxify oxygen radicals or inhibit the pathomechanisms leading to the enhanced radical generation. Hopefully, the combination of early revascularization with these already available scavengers will improve the high mortality and morbidity of patients suffering from intestinal ischemia.
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PMID:Oxygen radicals in intestinal ischemia and reperfusion. 222 27