Elevated level of renal xanthine oxidase mRNA transcription after nephropathogenic infectious bronchitis virus infection in growing layers

Lin, Huayuan; Huang, Qiqi; Guo, Xiaoquan; Liu, Ping; Liu, Weilian; Zou, Yuelong; Zhu, Shuliang; Deng, Guangfu; Kuang, Jun; Zhang, Caiying; Cao, Huabin; Hu, Guoliang

XOD can oxidize a variety of purines, pyrimidines, pteridines, and other heterocyclic nitrogenous compounds while concomitantly generating UA, superoxide anion (O 2 − ) and hydrogen peroxide (H 2 O 2 ). It is well known that appropriate concentrations of UA and reactive oxygen species (ROS) are necessary for maintenance of homeostasis. Previous studies have shown that hyperactivity of XOD occasionally occurs in the body, and that by-products of both UA and ROS play important roles in various pathophysiological conditions [2] . Peralta et al. [22] demonstrated that XOD activity induced by hepatic ischemia-reperfusion was associated with liver and lung damage. Among human diseases, gout or hyperuricemia was also associated with the activity of XOD, and this enzyme has become a target of drugs used for therapy [20] . Therefore, its activity plays an important role in the development of several diseases. Former studies have shown that infection with NIBV could induce elevation of serum UA in chickens [1] . However, few studies have been conducted to explain the relationships between XOD and hyperuricemia induced by NIBV in the poultry industry to date.