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Florfenicol induces renal toxicity in chicks by promoting oxidative stress and apoptosis

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Abstract

To explore the mechanism of renal toxicity induced by florfenicol (FFC), 120 chicks were randomly divided into 6 groups, 20 in each group. Except for the control group, different doses of FFC (0.15 g/L, 0.3 g/L, 0.6 g/L, 1.2 g/L, and 1.8 g/L) were added to drinking water in the other 5 groups. Five days later, blood was collected from the vein under the wing, and the complete kidneys were obtained as soon as possible, then tested the experimental indicators. The results showed that compared with control group, all doses of FFC significantly reduced the average weight gain of chicks (P < 0.05 or P < 0.01). Except for the 0.15 g/L FFC group, kidney index of chicks in the other doses of FFC groups were significantly increased (P < 0.05 or P < 0.01). The kidney tissues in all FFC groups showed obvious damage, deformities, cell atrophy, and cell gap enlargement. In addition, all doses of FFC significantly increased the contents of uric acid (UA), blood urea nitrogen (BUN), creatinine (CRE) in serum, and malondialdehyde (MDA) in renal tissue (P < 0.05 or P < 0.01), but significantly reduced the levels of glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in renal tissue (P < 0.05 or P < 0.01). FFC significantly inhibited the mRNA and protein expression levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase-1 (NQO-1), and increased the mRNA and protein expression levels of p53, Caspase-3, and Caspase-6 (P < 0.05 or P < 0.01). The apoptotic rate of renal cells in all doses of FFC groups increased significantly (P < 0.05 or P < 0.01). It was concluded that FFC had a certain degree of nephrotoxicity, and with the increase of FFC concentration, the kidney injury of chicks became more and more serious. FFC promoted oxidative stress response in kidney of chicks by inhibiting the expression of related factors in Nrf2-ARE pathway. Moreover, the expression of pro-apoptotic factors was upregulated to improve the apoptosis rate of renal cells, which resulted in excessive apoptosis of renal cells and seriously affected the kidney function of chicks.

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Funding

This study was financially supported by Subsidized Project for Cultivating Innovative Ability of Postgraduates of Hebei province (NO.CXZZBS2019096).

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Wanyu Shi and Yongzhan Bao conceived and designed the study, and they rigorously revised the manuscript. Xiao Wang and Chao Han participated in the design of the experiment, conducted most of the experiments, and analyzed the results. They also co-wrote the manuscript. Yumeng Geng and Yuanyuan Wei helped collect samples and participated in the qPCR experiment. Yuqing Cui participated in the H&E, Western blot, and TUNEL experiments. All authors read and approved the final manuscript.

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Correspondence to Wanyu Shi or Yongzhan Bao.

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Responsible editor: Mohamed M. Abdel-Daim

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Wang, X., Han, C., Cui, Y. et al. Florfenicol induces renal toxicity in chicks by promoting oxidative stress and apoptosis. Environ Sci Pollut Res 28, 936–946 (2021). https://doi.org/10.1007/s11356-020-10550-4

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