NiCl2-Down-Regulated Antioxidant Enzyme mRNA Expression Causes Oxidative Damage in the Broiler-/sup>s Kidney

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• 作者：Hongrui Guo (1)
  Bangyuan Wu (1)
  Hengmin Cui (1) (2)
  Xi Peng (1) (2)
  Jing Fang (1) (2)
  Zhicai Zuo (1) (2)
  Junliang Deng (1) (2)
  Xun Wang (1) (2)
  Jie Deng (1)
  Shuang Yin (1)
  Jian Li (1)
  Kun Tang (1)
  
• 关键词：NiCl2 ; Oxidative damage ; Antioxidant enzymes ; mRNA expression ; Kidney ; Broiler
• 刊名：Biological Trace Element Research
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：162
• 期：1-3
• 页码：288-295
• 全文大小：526 KB
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  14. Wu B, Cui H, Peng X, Fang J, Zuo Z, Deng J et al (2014) Dietary nickel chloride induces oxidative stress, apoptosis and alters Bax/Bcl-2 and caspase-3 mRNA expression in the cecal tonsil of broilers. Food Chem Toxicol 63:18-9. doi:10.1016/j.fct.2013.10.033 CrossRef
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• 作者单位：Hongrui Guo (1)
  Bangyuan Wu (1)
  Hengmin Cui (1) (2)
  Xi Peng (1) (2)
  Jing Fang (1) (2)
  Zhicai Zuo (1) (2)
  Junliang Deng (1) (2)
  Xun Wang (1) (2)
  Jie Deng (1)
  Shuang Yin (1)
  Jian Li (1)
  Kun Tang (1)
  
  1. Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Yaan, China
  2. College of Veterinary Medicine, Sichuan Agricultural University, Yaan, Sichuan, China, 625014
  
• ISSN：1559-0720

文摘

The kidney serves as a major organ of nickel (Ni) excretion and is a target organ for acute Ni toxicity due to Ni accumulation. There are no studies on the Ni or Ni compound-regulated antioxidant enzyme mRNA expression in animals and human beings at present. This study was conducted to investigate the pathway of nickel chloride (NiCl2)-caused renal oxidative damage by the methods of biochemistry, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Two hundred and eighty one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900?mg/kg of NiCl2 for 42?days. Dietary NiCl2 elevated the malondialdehyde?(MDA), nitric oxide?(NO), 8-hydroxy-2'-deoxyguanosine?(8-OHdG) contents, and reduced the ability to inhibit hydroxy radical in the NiCl2-treated groups. Also, the renal inducible nitric oxide synthase?(iNOS) activity and mRNA expression levels were increased. The total antioxidant?(T-AOC) and activities of antioxidant enzymes including copper zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glutathione-s-transferase (GST) were decreased, and the glutathione?(GSH) contents as well were decreased in the kidney. Concurrently, the renal CuZn-SOD, Mn-SOD, CAT, GSH-Px, GST, and GR mRNA expression levels were decreased. The above-mentioned results showed that dietary NiCl2 in excess of 300?mg/kg caused renal oxidative damage by reducing mRNA expression levels and activities of antioxidant enzymes, and then enhancing free radicals generation, lipid peroxidation, and DNA oxidation.