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 is a molybdenum iron-sulfur flavin hydroxylase that is widely distributed in most animal species [8, 28] . Beedkar et al. [5] demonstrated that XOD was a vital mediator in the pathogenesis of human gout. In addition to the generation of uric acid, XOD can catalyze the substrate and concomitant generation of oxygen radicals, which can then induce tissue damage. There is mounting evidence that increased XOD activity is correlated with the development of many diseases due to the concomitantly increased production of uric acid and free radicals [6, 16] . However, to prevent tissue damage caused by oxidative stress, the major antioxidant enzymes such as superoxide dismutases (SOD) and glutathione peroxidase (GSH-PX) played an important role in maintaining the balance between antioxidants and oxidation in vivo [17, 27] . Tas et al. [31] reported that increased activities of SOD and GSH-PX could reduce the oxidative damage induced by reactive oxygen species (ROS) in rats. However, few studies have investigated the relationships among XOD, antioxidants and gout induced by NIBV. In the present study, chickens were infected with NIBV and changes in the renal XOD mRNA transcript level, serum XOD, serum uric acid and antioxidant levels were evaluated to clarify the dynamic characteristics of XOD and antioxidants in chickens after infection with NIBV.