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

The role of xanthine oxidase (XO) in the interferon (IFN)-dependent modulation of the hepatic cytochrome P-450 system was assessed in SENCAR mice. Intraperitoneal administration of 10(4)-10(5) units of IFN-gamma resulted in dose-dependent increases in hepatic XO activities. XO activity was significantly elevated within 12 h of IFN-gamma treatment, and reached a maximum between 24-48 h, and returned to basal levels within 72-96 h. Although the kinetics of increase and decline of XO activity correlated with the loss and subsequent recovery of hepatic P-450 levels, there was no quantitative correlation between hepatic XO activity and P-450 content. Comparable results were obtained in mice pretreated with the P-450 inducer Aroclor 1254 3 days prior to IFN-gamma administration. The increases in XO activity following IFN-gamma treatment were the consequence of increases in xanthine dehydrogenase (XD), and the conversion of XD to XO. The ad libitum administration of allopurinol to IFN-gamma-treated mice reduced XO specific activity to approximately 4% of the basal activity of control mice, but did not prevent reductions in cytochrome P-450 levels or the activities of two P-450 dependent monooxygenases. Collectively, these data suggest that the reductions in the hepatic P-450 system noted after IFN administration are not a consequence of elevated XO activities.
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PMID:Coordinate modulation of murine hepatic xanthine oxidase activity and the cytochrome P-450 system by interferons. 169 64

Ethanol ingestion causes an increase in free radical generation in the liver mainly by induction of microsomal cytochrome P-450, conversion of xanthine dehydrogenase into xanthine oxidase in cytosol and increased one electron oxygen reduction in mitochondria. As a result, the decrease in antioxidant status characterized by changes in activity of antioxidant enzymes and by decrease in nonenzymatic antioxidant level with different intensification depended on acute or chronic alcohol ingestion. The consequence of the above changes is oxidative stress in the liver. It intensifies free radical action on cell compartments which are characterized by oxidative modification of lipids, proteins and nucleic acids. These cytotoxic processes may finally lead to alcoholic liver injury in the end.
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PMID:[Influence of ethanol on oxidative stress in the liver]. 1263 27