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    周华芳, 张金雷, 卢秀娟, 阮文丽, 吴红玲. 亚慢性砷暴露对大鼠脑组织氧化应激和γ-谷氨酰半胱氨酸合成酶表达影响[J]. 环境卫生学杂志, 2016, 6(2): 102-105,109. DOI: 10.13421/j.cnki.hjwsxzz.2016.02.003
    引用本文: 周华芳, 张金雷, 卢秀娟, 阮文丽, 吴红玲. 亚慢性砷暴露对大鼠脑组织氧化应激和γ-谷氨酰半胱氨酸合成酶表达影响[J]. 环境卫生学杂志, 2016, 6(2): 102-105,109. DOI: 10.13421/j.cnki.hjwsxzz.2016.02.003
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    ZHOU Huafang, ZHANG Jinlei, LU Xiujuan, RUAN Wenli, WU Hongling. Effect of Sub-chronic Arsenic Exposure on Expression of γ-Glutamylcysteine Synthetase (γ-GCS) and Oxidative Stress in Rats Brain[J]. Journal of Environmental Hygiene, 2016, 6(2): 102-105,109. DOI: 10.13421/j.cnki.hjwsxzz.2016.02.003
    Citation: ZHOU Huafang, ZHANG Jinlei, LU Xiujuan, RUAN Wenli, WU Hongling. Effect of Sub-chronic Arsenic Exposure on Expression of γ-Glutamylcysteine Synthetase (γ-GCS) and Oxidative Stress in Rats Brain[J]. Journal of Environmental Hygiene, 2016, 6(2): 102-105,109. DOI: 10.13421/j.cnki.hjwsxzz.2016.02.003
    shu

    亚慢性砷暴露对大鼠脑组织氧化应激和γ-谷氨酰半胱氨酸合成酶表达影响

    Effect of Sub-chronic Arsenic Exposure on Expression of γ-Glutamylcysteine Synthetase (γ-GCS) and Oxidative Stress in Rats Brain

      摘要
    • 摘要:
      目的  观察亚慢性砷暴露对大鼠脑组织抗氧化能力影响及γ-GCS表达变化,探讨砷暴露致神经损害机制。
      方法  采用40只清洁级SD大鼠(体重:100 g±20 g),随机分为4组,即对照组(蒸馏水)、低剂量组(2.4 mg/L NaAsO2溶液)、中剂量组(12 mg/L NaAsO2溶液)和高剂量组(60 mg/L NaAsO2溶液),每组10只,雌雄各半。以自由饮水方式染砷100 d。采用电感耦合等离子体发射光谱法(ICP-AES)测定脑砷含量;比色法测定脑组织总抗氧化能力;微量测试法测定脑海马组织GSH浓度;实时荧光定量(qRT-PCR)测定海马γ-GCS mRNA;免疫组化法测定γ-GCS蛋白的表达。
      结果  染砷组与对照组比较:染砷组体重差异无统计学意义(P>0.05)、脑组织砷含量增高、总抗氧化能力下降、海马组织谷胱甘肽浓度降低,差异均有统计学意义(P<0.05);染砷组大鼠海马区γ-GCS mRNA表达下调、γ-GCS蛋白表达下降,差异均有统计学意义(P<0.05)。
      结论  亚慢性砷暴露可导致脑组织氧化损伤,诱发氧化应激及γ-GCS 表达降低,从而使脑组织中GSH水平下降。

       

      Abstract:
      Objectives  To observe the effect of sub-chronic arsenic exposure on antioxidant ability and the expression of γ-glutamylcysteine synthetase (γ-GCS) in brain of rats, in order to discuss the mechanism of the damage in nerve system.
      Methods  Forty SD rats (body weight:100g±20g; half male and half female)were randomly divided into four groups: one control group and three treated groups (treated with NaAsO2 in drinking water at dosages of 2.4 mg/L, 12 mg/L and 60 mg/L, respectively). The level of arsenic in brain tissue was detected with ICP-OES; total antioxidant ability in brain tissue was tested by colorimetry;level of GSH in hippocampus was measured by trace test method; the expression of γ-GCS mRNA in hippocampus was checked by qRT-PCR technique; the expression of γ-GCS protein in hippocampus was observed by immunohistochemistry.
      Results  There were no significant differencs on body weight of rats between the control and treated groups (P>0.05). The levels of arsenic in brain of treated groups were increased; the total antioxidant abilities in brain of treated groups were decreased, the level of GSH in hippocampus of treated groups were decreased, the expression of γ-GCS mRNA and γ-GCS protein in hippocampusof treated groups were down regulated (P<0.05).
      Conclusions  Sub-chronic arsenic exposure in rats could induce oxidative damage in brain, induce oxidative stress and downregulate the expression of γ-GCS mRNA in hippocampus, thereby, reduce the level of GSH in hippocampus.

       

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