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Arsenic and/or copper caused inflammatory response via activation of inducible nitric oxide synthase pathway and triggered heat shock protein responses in testis tissues of chicken

Shao, Yizhi, Zhao, Hongjing, Wang, Yu, Liu, Juanjuan, Li, Jinglun, Chai, Hongliang, Xing, Mingwei
Environmental science and pollution research international 2018 v.25 no.8 pp. 7719-7729
arsenic, arsenic oxide, chickens, copper, copper sulfate, cytokines, heat shock proteins, histology, inducible nitric oxide synthase, inflammation, males, messenger RNA, poisoning, protective effect, subchronic exposure, testes, tissues
The aim of this study is to investigate the effects of arsenic (As) and copper (Cu) on the inflammatory response, and the protective roles of heat shock proteins (Hsps) in chicken testes. Seventy-two 1-day-old male Hy-line chickens were treated with 30 mg/kg feed of arsenic trioxide (As₂O₃) and/or 300 mg/kg feed of copper sulfate (CuSO₄) for 4, 8, and 12 weeks. The histological changes, inducible nitric oxide synthase (iNOS) activity, and the expressions of Hsps and inflammatory cytokines were detected. The results showed that slight histology changes were obvious in the testis tissue exposure to treatment groups. The activity and the protein level of iNOS were increased compared to the control group. The mRNA levels of proinflammatory cytokines and inflammatory factors were increased as a whole. However, anti-inflammatory cytokines were inhibited. The mRNA and protein levels of Hsp60, Hsp70, and Hsp90 were upregulated. These results suggested that sub-chronic exposure to As and/or Cu induced testicular poisoning in chickens. Increased Hsps tried to protect chicken testis tissues from tissues damage caused by inflammation. In conclusion, testicular poisoning induced by As and/or Cu caused inflammatory response and heat shock protein response in chicken testis tissues.