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作 者:闫铭锋[1] 王秋英 王宁[1] 吴喜江 罗琴[1] 宣小强 任秀芳 王晓怀[1] 祁光伟 程宁[1]
机构地区:[1]兰州大学甘肃省新药临床前研究重点实验室,兰州730000 [2]金川公司职工医院
出 处:《卫生研究》2012年第4期632-635,共4页Journal of Hygiene Research
基 金:金川集团公司与兰州大学产学研合作项目
摘 要:目的通过研究大鼠急性羰基镍中毒肝组织中丙二醛(MDA)、抗超氧阴离子及诱导型一氧化氮合酶(iNOS)含量的变化,探讨急性羰基镍中毒肝脏损伤机制。方法 SD大鼠静态吸入不同浓度羰基镍染毒(低剂量组20mg/m3,中剂量组135mg/m3,高剂量组250mg/m3),并设氯气染毒组(250mg/m3)和正常对照组(未作处理),染毒后不同时间(染毒后第1天,第2天,第3天及第7天)取材,应用化学显色法测定肝组织中MDA、抗超氧阴离子和iNOS的含量。结果 250mg/m3染毒组大鼠肝脏中MDA和抗超氧阴离子含量升高与20mg/m3、135mg/m3羰基镍组间存在明显差异(P<0.01);135mg/m3、250mg/m3组的iNOS含量升高与20mg/m3染毒组及正常对照组都存在明显差异(P<0.05)。结论急性羰基镍中毒可诱发肝组织明显氧化应激,且存在明显的剂量-效应关系(P<0.01)。Objective To investigate the level of malondiadehyde (MDA), antisuperoxide anion and inducible nitric oxide synthase (iNOS) in liver of rats poisoned by nickel carbonyl in order to discuss the mechanism of acute nickel earbonyl poisoning. Methods Healthy SD rats were intoxicated acutely by different concentrations of nickel earbonyl (20, 135 and 250mg/m3 for low, middle and high dose groups, respectively). SD rats inhaled by chlorine (250mg/m3 for chlorine group) were used as positive control group and other healthy SD rats as normal control group. Liver of animals was taken at different time points after exposure. The levels of MDA, iNOS and antisuperoxide anion were detected by biochemical assay. Results The contents of MDA and antisuperoxide anion in the liver of high dose group were significantly higher than that of other exposed groups and control group (P 〈 0.01 ). The contents of iNOS in middle and high dose group were higher than that in low dose group and control group (P 〈 0.05). Conclusion The oxidative damage in the liver of SD rats could be induced by carbonyl nickel in air with increasing concentrations and in an obvious dose-response relationships.
关 键 词:羰基镍 氯气 丙二醛 诱导型一氧化氮合酶 抗超氧阴离子
分 类 号:R135.1[医药卫生—劳动卫生] Q593.1[医药卫生—公共卫生与预防医学]
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