title: Immunology of pyelonephritis. VII. Effect of allopurinol.
abstract: The inflammatory response and the respiratory burst of bacterial phagocytosis have been shown to be at least partially responsible for the renal damage from infection. In addition, we have shown that renal blood flow decreases following infection. Hypoxanthine is produced in ischemic tissue during the anaerobic metabolism of adenosine monophosphate (AMP). During reperfusion hypoxanthine is metabolized to uric acid and superoxide in the presence of xanthine oxidase. The toxicity of this oxygen radical was prevented by preventing its formation with pretreatment with allopurinol, an xanthine oxidase inhibitor. The data suggest that xanthine oxidase may be the enzyme responsible for the respiratory burst of phagocytosis, as well as preventing reperfusion damage which occurs after ischemia.
mesh_terms: D000249:Adenosine Monophosphate / Q000378:metabolism; D000493:Allopurinol / Q000627:therapeutic use*; D000818:Animals; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D005260:Female; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008252:Macaca fascicularis; D010587:Phagocytosis; D011704:Pyelonephritis / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D007042:Hypoxanthines; D019271:Hypoxanthine; D000249:Adenosine Monophosphate; D000493:Allopurinol; D014969:Xanthine Oxidase