Nickel-induced oxidative stress and effect of antioxidants in human lymphocytes
Nickel-induced oxidative stress and effect of antioxidants in human lymphocytes
复制标题
DOI：
10.1007/s00204-002-0427-6
复制
发表时间：
2003-03-01
影响因子：
6.1
通讯作者：
Yen, SF
中科院分区：
文献类型：
--
作者：
Chen, CY;Wang, YF;Yen, SF
本研究的目的是评估急性镍（Ni）处理1 h后人淋巴细胞的氧化效应;细胞内活性氧（ROS）、脂质过氧化（LPO）和羟基自由基（（OH）-O-）水平。在分离的淋巴细胞中检查。抗氧化剂的潜在影响也进行了研究。急性处理后，NiCl 2（0-10 mM）显着降低淋巴细胞的活力。NiCl 2似乎以浓度依赖性方式增加二氯荧光素（DCF）荧光的程度和体外人淋巴细胞中硫代巴比妥酸反应物质（TBARS）的水平：（OH）-O-的水平。通过两种主要的羟基化衍生物，2，3-和2，5-二羟基苯甲酸酯（DHB）进行定量。镍处理组的2，3-和2，5-DHB水平显著高于对照组。过氧化氢酶部分降低了NiCl 2诱导的氧化剂和TBARS的升高，而超氧化物歧化酶（SOD）提高了氧化剂和TBARS的水平。谷胱甘肽（GSH）和甘露醇均能显著抑制NiCl 2诱导的荧光和LPO。NiCl 2诱导的（OH）-O-生成增加。过氧化氢酶、GSH和甘露醇可显著抑制SOD的活性。这些结果表明，NiCl_2诱导的淋巴细胞毒性可能是由氧自由基中间体介导的，其中（OH）-O-的产生加速。可能在镍诱导的人淋巴细胞氧化损伤中起重要作用。过氧化氢酶、GSH和甘露醇各自提供针对由Ni诱导的氧化应激的保护。
The purpose of this study was to evaluate the oxidative effect in human lymphocytes after acute nickel (Ni) treatment for 1 h; levels of intracellular reactive oxygen species (ROS), lipid peroxidation (LPO) and hydroxyl radicals ((OH)-O-.) were examined in isolated lymphocytes. The potential effects of antioxidants were also examined. After acute treatment, NiCl2 (0-10 mM) significantly decreased the viability of lymphocytes. NiCl2 appear to increase the degree of dichlorofluorescein (DCF) fluorescence and the levels of thiobarbituric acid-reactive substances (TBARS) in human lymphocytes in vitro in a concentration-dependent manner: The level of (OH)-O-. was quantified by two main hydroxylated derivates, 2,3- and 2,5-dihydroxybenzate (DHB). Levels of 2,3- and 2,5-DHB were significantly higher in the Ni-treated group than in controls. Catalase partially reduced the NiCl2-induced elevation of oxidants and TBARS, whereas superoxide dismutase (SOD) enhanced the level of oxidants and TBARS. Both NiCl2-induced fluorescence and LPO were prevented significantly by glutathione (GSH) and mannitol. NiCl2-induced increase in generation of (OH)-O-. was prevented significantly by catalase, GSH and mannitol, but not by SOD. These results suggest that NiCl2-induced lymphocyte toxicity may be mediated by oxygen radical intermediates, for which the accelerated generation of (OH)-O-. may plays an important role in Ni-induced oxidative damage of human lymphocytes. Catalase, GSH and mannitol each provides protection against the oxidative stress induced by Ni.