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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.