【作者】 郭红瑞； 吴邦元； 崔恒敏； 彭西； 方静； 左之才； 邓俊良； 王讯； 邓婕； 银霜； 李剑； 唐堃；

【Author】 GUO Hongrui;WU Bangyuan;CUI Hengmin;PENG Xi;FANG Jing;ZUO Zhicai;DENG Junliang;WANG Xun;DENG Jie;YIN Shuang;LI Jian;TANG Kun;Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province;College of Veterinary Medicine, Sichuan Agricultural University;

【机构】 四川省环境公害与动物疾病重点实验室； 四川农业大学动物医学院；

【摘要】 本研究旨在探究氯化镍(Ni Cl2)诱导雏鸡肾脏氧化损伤的机制。选用1日龄肉鸡健雏280只,随机分为4组,每组70只,分别饲喂对照日粮和添加300 mg/kg,600 mg/kg,900 mg/kg氯化镍的日粮,试验周期6周。14、28和42日龄时每组随机抽取5只肉鸡,取出肾脏,应用生化,荧光定量PCR和ELISA方法观测氯化镍对雏鸡肾脏抗氧化系统的影响。结果表明,饲喂氯化镍日粮后雏鸡肾脏中丙二醛(MDA),一氧化氮(NO),8羟基脱氧鸟苷(8-Ohd G)显著增加(P<0.05或P<0.01),抑制羟自由基的能力显著降低(P<0.05或P<0.01)。肾脏中总抗氧化能力(T-AOC),铜锌超氧化物歧化酶(Cu Zn-SOD),锰超氧化物歧化酶(Mn-SOD),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSH-Px),谷胱甘肽还原酶(GR),谷胱甘肽-S-转移酶(GST)的活性和还原性谷胱甘肽(GSH)的含量显著降低(P<0.05或P<0.01),诱导型一氧化氮合成酶(i NOS)活性显著升高(P<0.05或P<0.01)。同时,i NOS m RNA水平显著升高,Cu Zn-SOD、Mn-SOD、CAT、GSH-Px、GR、GST的m RNA水平显著降低(P<0.05或P<0.01)。上述结果表明,日粮中氯化镍含量超过300 mg/kg导致肾脏的氧化损伤,其机制是肾脏抗氧化酶的基因表达和活性降低,引起自由基、脂质过氧化物聚集和DNA损伤所致。更多还原

【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 m RNA 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（q RT-PCR） and enzyme-linked immunosorbent assay（ELISA）. Two hundred and eighty one-day-old broilers were randomly divided intofour groups and fed on a control diet and three experimental diets supplemented with 300, 600 and 900mg/kg of NiCl₂ for 42 days. Dietary NiCl₂ significantly elevated（P<0.05 or P<0.01） the malondialdehyde（MDA）, nitric oxide（NO）, 8-hydroxy-2’-deoxyguanosine（8-OHd G） contents, and significantly reduced（P<0.05 or P<0.01） the ability to inhibit hydroxy radical in the NiCl₂-treated groups. Also, the renal inducible nitric oxide synthase（i NOS） activity and m RNA expression levels were significantly increased（P<0.05 or P<0.01）. The total antioxidant（T-AOC） and activities of antioxidant enzymes including copper zinc superoxide dismutase（Cu Zn-SOD）, manganese superoxide dismutase（Mn-SOD）, catalase（CAT）,glutathione peroxidase（GSH-Px）, glutathione reductase（GR） and glutathione-s-transferase（GST） were significantly decreased（P<0.05 or P<0.01） as well as the glutathion（GSH） contents were significantly decreased（P<0.05 or P<0.01） in the kidney. Concurrently, the renal Cu Zn-SOD, Mn-SOD, CAT, GSH-Px,GST and GR m RNA expression levels were significantly decreased（P<0.05 or P<0.01）. The above-mentioned results showed that dietary NiCl₂ in excess of 300 mg/kg caused renal oxidative damage by reducing m RNA expression levels and activities of antioxidant enzymes, and then enhancing free radicals generation, lipid peroxidation and DNA oxidation.更多还原