Abstract
As the end‐product of purine degradation, uric acid is generated in the xanthine/hypoxanthine reactions catalyzed by xanthine oxiodreductase (XOR). The purpose of this first study was to determine the effects of allopurinol and inosine on XOR activity in liver.In the first study, Cobb x Cobb (n=15; 5weeks old) were separated into three treatments (n=5); control (CON), INO (inosine at .6M/kg feed), or INOAL (inosine and allopurinol 50mg/kgBW). INOAL birds had a significantly lower (p=0.005) uric acid concentration in the liver. In the second study, Cobb x Cobb broilers (n=12; 4 weeks old) were separated into two treatments (n=6); control (CON) and AL (allopurinol 35mg/kg BW). The purpose of this study was to assess mitochondrial function in broiler chickens in response to potential oxidative stress from administration of allopurinol. Mitochondria were freshly isolated from liver tissue and assessed for State III and State IV respiration using polarography. There was a significant reduction in State III respiration (p=0.01) and State IV respiration (p=0.007) in allopurinol‐treated birds compared to the control. The reduced uric acid concentration in the liver suggests that there is a residual effect of allopurinol, which potentially results in lowered antioxidant activity in this tissue thereby causing an increase in oxidative stress within this tissue and can result in mitochondrial dysfunction.
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