title: NiCl2-down-regulated antioxidant enzyme mRNA expression causes oxidative damage in the broiler(')s kidney.
abstract: 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.
authors.affiliation: Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Yaan, China.
authors.forename: Hongrui
authors.initials: H
authors.lastname: Guo
authors.forename: Bangyuan
authors.initials: B
authors.lastname: Wu
authors.forename: Hengmin
authors.initials: H
authors.lastname: Cui
authors.forename: Xi
authors.initials: X
authors.lastname: Peng
authors.forename: Jing
authors.initials: J
authors.lastname: Fang
authors.forename: Zhicai
authors.initials: Z
authors.lastname: Zuo
authors.forename: Junliang
authors.initials: J
authors.lastname: Deng
authors.forename: Xun
authors.initials: X
authors.lastname: Wang
authors.forename: Jie
authors.initials: J
authors.lastname: Deng
authors.forename: Shuang
authors.initials: S
authors.lastname: Yin
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.forename: Kun
authors.initials: K
authors.lastname: Tang
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D002645:Chickens; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism; D009532:Nickel / Q000494:pharmacology*; D010084:Oxidation-Reduction / Q000187:drug effects; D012333:RNA, Messenger; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D012333:RNA, Messenger; D008315:Malondialdehyde; C022838:nickel chloride; D009532:Nickel; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D003849:Deoxyguanosine