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NiCl2-Down-Regulated Antioxidant Enzyme mRNA Expression Causes Oxidative Damage in the Broiler’s Kidney
- Guo, Hongrui, Wu, Bangyuan, Cui, Hengmin, Peng, Xi, Fang, Jing, Zuo, Zhicai, Deng, Junliang, Wang, Xun, Deng, Jie, Yin, Shuang, Li, Jian, Tang, Kun
- Biological trace element research 2014 v.162 no.1-3 pp. 288-295
- DNA, antioxidant activity, antioxidants, catalase, dietary supplements, enzyme-linked immunosorbent assay, excretion, experimental diets, free radicals, gene expression, glutathione, glutathione peroxidase, glutathione transferase, glutathione-disulfide reductase, humans, inducible nitric oxide synthase, kidneys, lipid peroxidation, malondialdehyde, messenger RNA, nickel, nitric oxide, oxidation, quantitative polymerase chain reaction, superoxide dismutase, toxicity, zinc
- 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 NiCl₂for 42 days. Dietary NiCl₂elevated 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 NiCl₂in 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.