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The aim of the study is to investigate the effects of sub-chronic poisoning with arsenic on the testes of chickens treated. Seventy-two 1-day-old chickens were randomly divided into 4 groups and provided food with different doses arsenic. The histological changes were examined. The mRNA levels of inflammatory factors, including transcription factor nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E synthase (PTGEs), and heat shock proteins (Hsps), including Hsp70, Hsp90, Hsp60, Hsp40, and Hsp27 were assessed by quantitative real-time PCR in the testes of chickens. The protein expressions of iNOS, Hsp60, and Hsp70 were detected by western blot. Increased mRNA and protein levels of inflammatory factors and Hsps with testicular damage showed that arsenic-induced testicular toxicity includes inflammatory and heat shock response in chickens, and that increased Hsps levels may play a protective role in inflammation damage induced by arsenic on the testes of chickens. [ABSTRACT FROM AUTHOR]

Background: The heavy metal arsenic is widely distributed in nature and posses a serious threat to organism's health. However, little is known about the arsenic-induced inflammatory response in the brain tissues of birds and the relationship and mechanism of the inflammatory response. The purpose of this study was to explore the effects of dietary arsenic on the expression of inflammatory cytokines in the brains of Gallus gallus. Results: Seventy-two 1-day-old male Hy-line chickens were divided into a control group, a low arsenic trioxide (As2O3)-treated (7.5 mg/kg) group, a middle As2O3-treated (15 mg/kg) group, and a high As2O3-treated (30 mg/kg) group. Arsenic exposure caused obvious ultrastructural changes. The mRNA levels of the transcription factor nuclear factor-κB (NF-κB) and of pro-inflammatory cytokines, including inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E synthase (PTGEs), in chicken brain tissues (cerebrum, cerebellum, thalamus, brainstem and myelencephalon) on days 30, 60 and 90, respectively, were measured by real-time PCR. The protein expression of iNOS was detected by western blot. The results showed that after being treated with As2O3, the levels of inflammatory-related factor NF-κB and pro-inflammatory cytokines in chicken brain tissues increased (P < 0.05). Conclusions: Arsenic exposure in the chickens triggered host defence and induced an inflammatory response by regulating the expression of inflammatory-related genes in the cerebrum, cerebellum, thalamus, brainstem and myelencephalon. These data form a foundation for further research on arsenic-induced neurotoxicity in Gallus gallus. [ABSTRACT FROM AUTHOR]