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Circulating xanthine oxidase in human ischemia reperfusion
1Department of Pediatrics, University of Alabama at Birmingham 35233, USA.
Southern Medical Journal
|April 1, 1995
Summary
Ischemia-reperfusion releases xanthine oxidase (XO) and xanthine dehydrogenase (XDH) into circulation. This release of reactive oxygen species (ROS) may explain organ damage following liver and intestinal ischemia.
Area of Science:
- Biochemistry
- Physiology
- Pathology
Background:
- Reactive oxygen species (ROS) contribute to ischemia-induced injury.
- Xanthine oxidase (XO) is a primary source of ROS.
- The role of XO and xanthine dehydrogenase (XDH) release during ischemia-reperfusion is not fully understood.
Purpose of the Study:
- To investigate the release of XO and XDH into circulation during ischemia-reperfusion of the human liver and intestine.
- To quantify the enzymatic activity of XO and XDH in plasma following aortic cross-clamp procedures.
Main Methods:
- Blood samples were collected from a patient before and after aortic cross-clamp.
- Plasma was incubated with xanthine to measure XDH+XO and XO activity.
- Urate formation was quantified using high-performance liquid chromatography (HPLC).
Main Results:
- XDH+XO and XO activities significantly increased after reperfusion of the superior mesenteric, celiac, and right renal arteries.
- Enzymatic activities rose from baseline levels (1.88 and 1.66 microU/mg protein) to post-reperfusion levels (3.77 and 3.11 microU/mg protein) within 7 minutes.
- A significant release of ROS-generating enzymes into circulation was observed.
Conclusions:
- Ischemia-reperfusion leads to the release of XO and XDH into the bloodstream.
- This enzyme release represents a significant source of ROS.
- The findings suggest a mechanism for observed lung or heart damage after liver and intestinal ischemia.