Abstract
Summary
Certain aspects of the xanthine oxidase hypothesis of atherosclerosis were studied. Xanthine oxidase activity was determined by liquid scintillation counting of [14C]uric acid formed by the action of the enzyme on [14C]xanthine. Results show that the proposal that xanthine oxidase passes through the stomach and is absorbed intact by the small intestine is implausible. The treatment of milk with a low pH buffer resulted in irreversible loss of xanthine oxidase activity. The incubation of everted rat intestine in buffer and in buffer-milk mixtures showed no difference in enzyme activity in serosal fluid or in intestinal homoge-nates.
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