大鼠急性羰基镍中毒脑组织氧化应激的研究

Oxidative stress in brain tissue of rats poisoned by acute nickel carbonyl

目的通过观察大鼠急性羰基镍中毒脑组织中总一氧化氮合酶(T-NOS)、诱导型一氧化氮合酶(iNOS)和抗超氧阴离子含量的变化,探讨羰基镍的神经毒性机制。方法采用健康SD大鼠静态吸入方式染毒,羰基镍染毒浓度分别为20、135和250mg/m3,氯气染毒浓度为250mg/m3,染毒时间均为30min,并设正常对照组,染毒后第1、2、3和7天取脑组织。采用化学显色法测定不同组大鼠脑组织中T-NOS、iNOS和抗超氧阴离子的含量。结果 T-NOS含量在羰基镍各染毒组均出现升高,与正常对照组比较,差异均有统计学意义(P<0.01);20和250mg/m3羰基镍染毒组中T-NOS含量在第7天升高明显,与第1、2、3天之间比较,差异均有统计学意义(P<0.05)。iNOS含量在羰基镍染毒组和正常对照组间比较,差异无统计学意义(P>0.05),135和250mg/m3羰基镍染毒组间比较,差异有统计学意义(P<0.05)。抗超氧阴离子含量在羰基镍各染毒组均明显降低,与正常对照组比较,差异有统计学意义(P<0.05)。结论羰基镍可能通过诱导氧化应激反应产生神经毒性。

Objective To investigate the neurotoxicity of nickel carbonyl,changes of total nitric oxide sgnthase（T-NOS）,inducible nitric oxide synthase（iNOS）and anti-superoxide anion in brain tissue of rats with acute nickel carbonyl poisoning were observed.Methods Healthy SD rats were statically inhaled with nickel carbonyl of 20,135,and 250mg/m3 for 30min.Meanwhile,rats poisoned by chlorine gas with a concentration 250mg/m3 served as positive group,and healthy SD rats with no exposure were served as no-treatment negative group.The brain tissues of the rats were taken after 1st day,2nd day,3rd day,and 7th day after exposure respectively.The levels of T-NOS,iNOS and anti-superoxide anion were measured by colorimetry.Results Compared with the negative group,the level of T-NOS in the all nickel carbonyl poisoned groups increased and the difference was statistically significant（P〈0.01）.Whereas,the levels of anti-superoxide anion were significantly lower（P〈0.05）.The contents of T-NOS in 20 mg/m3 and 250mg/m3 of the exposed group increased significantly on the 7d,compared with other days（P〈0.05）.The content of iNOS showed no significant difference between nickel carbonyl poisoned groups and negative group（P〉0.05）,but it were significant difference between 135 mg/m3 and 250mg/m3 group（P〈0.05）.Conclusions Nickel carbonyl may induce neurotoxicity by oxidative stress in rat brains.