Abstract
Uric acid is generated in the xanthine/hypoxanthine reactions catalyzed by xanthine oxiodreductase (XOR) as the end‐product of purine degradation. The purpose of the first study was to determine the effects of allopurinol and inosine on XOR activity and gene expression in liver and kidney tissue. 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). Liver uric acid concentrations were reduced (p< 0.05). There was a significant (p 蠄 0.05) increase in XOR gene expression in the liver tissue of INOAL birds compared to CON and INO groups. There was no difference in XOR expression between treatments in kidney tissue. The purpose of the second study was to assess mitochondrial function. Cobb x Cobb broilers (n=12; 4 weeks old) were separated into two treatments (n=6); control (CON) and AL (allopurinol 35mg/kg BW). Mitochondria were freshly isolated from liver tissue and assessed for State III and State IV respiration using polarography. There was a reduction in State III respiration (p=0.01) and State IV respiration (p=0.007) in allopurinol‐treated birds compared to the control. Lowered uric acid in the liver can increase oxidative stress within this tissue subsequently resulting in mitochondrial dysfunction and an upregulation of XOR gene expression.
Published Version
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