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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 mechanism of acute carbonyl nickel poisoning in rats by studying the changes of malondialdehyde (MDA), superoxide anion and inducible nitric oxide synthase (iNOS) content in liver of acute carbonyl nickel poisoning rats. Methods SD rats were inhaled with different concentrations of nickel carbonyl (20mg / m3 in low dose group, 135mg / m3 in middle dose group, and 250mg / m3 in high dose group) (Untreated), different time after exposure (1st day, 2nd day, 3rd day and 7th day after exposure) were drawn. The contents of MDA, superoxide anion and iNOS in liver tissue were determined by chemical colorimetry Content. Results The increase of MDA and superoxide anion in the liver of 250mg / m3 group was significantly different from that of 20mg / m3 and 135mg / m3 carbonyl nickel group (P <0.01) There was a significant difference between iNOS content and 20mg / m3 exposure group and normal control group (P <0.05). Conclusion Acute carbonyl nickel poisoning can induce significant oxidative stress in liver tissue, and there is a significant dose-effect relationship (P <0.01).