Adenine nucleotide depletion from endothelial cells exposed to xanthine oxidase.

摘要: Hypoxia causes breakdown of cellular nucleotides, accumulation hypoxanthine (HX), and conversion xanthine dehydrogenase into oxidase (XO). Upon reoxygenation, the HX-XO reaction generates free radicals, one potential mechanism tissue damage. Because endothelial cells contain XO are exposed to circulating HX, they a likely target for We studied effect and/or HX at physiologically relevant concentrations on nucleotide metabolism cultured from human umbilical veins. Cells were labeled with [14C]adenine incubated up 6 h XO, or both, in absence presence serum. Adenine nucleotides cell extracts products (HX, xanthine, urate) medium separated counted. alone had no effect. (80 mU/ml) caused 70% (no serum) 40% (with fall adenine an equivalent increase urate. The combination 90% decrease energy charge, detachment culture plate. Nucleotide depletion was not accounted by proteolytic activity preparation. Albumin only half as effective serum preventing loss. Thus exogenous endogenous triggers catabolism, but is too low influence levels even high concentrations. Serum limits catabolic thus protects radical