Abstract

iclofenac sodium is a non-steroidal anti-inflammatory drug. After accidental exposure via food-chain of vultures feeding on livestock carcasses containing Diclofenac sodium residues leading to massive mortalities in vultures, its toxicity to avian has received widespread attention. In the present study, toxicity models of Diclofenac sodium to 30 specific-pathogen-free chickens aged 30 days were established through oral doses of 10 and 20 mg/kg, and its toxicological effects in duodenum tissues and intestinal microorganism of the chickens were explored. The results showed that Diclofenac sodium increased the content of uric acid, but decreased the activity of Xanthine oxidase indicating that its toxicity was more due to the obstruction of the urate excretion. Urate deposited in duodenum tissues induced the expression of nuclear factor erythroid-2 related factor, fas ligand, tumor necrosis factor-α, and tumor necrosis factor receptor superfamily member 1A, and caused severe edema, bleeding, villi shown broken and fallen off. In addition, after oral administration of Diclofenac sodium, the relative abundance of Proteobacteria and Bacteroidetes significantly increased while the relative abundance of Lactobacillales decreased. Diclofenac sodium disturbed the steady state of the intestinal environment leading to the proliferation of pathogenic bacteria but reduced the abundance of beneficial bacteria. The current research gave the toxicity evidence of Diclofenac sodium in duodenal tissue and intestinal microorganism.