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Dietary Nickel Chloride Induces Oxidative Intestinal Damage in Broilers

Author

Listed:
  • Bangyuan Wu

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Hengmin Cui

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Xi Peng

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Jing Fang

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Zhicai Zuo

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Junliang Deng

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

  • Jianying Huang

    (Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China)

Abstract

The purpose of this study was to investigate the oxidative damage induced by dietary nickel chloride (NiCl 2 ) in the intestinal mucosa of different parts of the intestine of broilers, including duodenum, jejunum and ileum. A total of 240 one-day-old broilers were divided into four groups and fed on a corn-soybean basal diet as control diet or the same basal diet supplemented with 300, 600 or 900 mg/kg NiCl 2 during a 42-day experimental period. The results showed that the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly ( p < 0.05 or p < 0.01) decreased in the 300, 600 and 900 mg/kg groups in comparison with those of the control group. In contrast, malondialdehyde (MDA) content was significantly ( p < 0.05 or p < 0.01) higher in the 300, 600 and 900 mg/kg groups than that in the control group. It was concluded that dietary NiCl 2 in excess of 300 mg/kg could cause oxidative damage in the intestinal mucosa in broilers, which finally impaired the intestinal functions including absorptive function and mucosal immune function. The oxidative damage might be a main mechanism on the effects of NiCl 2 on the intestinal health of broilers.

Suggested Citation

  • Bangyuan Wu & Hengmin Cui & Xi Peng & Jing Fang & Zhicai Zuo & Junliang Deng & Jianying Huang, 2013. "Dietary Nickel Chloride Induces Oxidative Intestinal Damage in Broilers," IJERPH, MDPI, vol. 10(6), pages 1-11, May.
    • Handle: RePEc:gam:jijerp:v:10:y:2013:i:6:p:2109-2119:d:25947
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    Citations

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    Cited by:

    1. Bangyuan Wu & Hengmin Cui & Xi Peng & Jing Fang & Zhicai Zuo & Junliang Deng & Jianying Huang, 2014. "Analysis of the Toll-Like Receptor 2-2 (TLR2-2) and TLR4 mRNA Expression in the Intestinal Mucosal Immunity of Broilers Fed on Diets Supplemented with Nickel Chloride," IJERPH, MDPI, vol. 11(1), pages 1-14, January.
    2. Jianying Huang & Hengmin Cui & Xi Peng & Jing Fang & Zhicai Zuo & Junliang Deng & Bangyuan Wu, 2013. "The Association between Splenocyte Apoptosis and Alterations of Bax, Bcl-2 and Caspase-3 mRNA Expression, and Oxidative Stress Induced by Dietary Nickel Chloride in Broilers," IJERPH, MDPI, vol. 10(12), pages 1-17, December.

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