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目的通过对羰基镍染毒大鼠心、脾、肾组织中超氧化物歧化酶(SOD)活力的动态观察,并比较不同脏器SOD活力变化的差异,探讨羰基镍的急性毒效应。方法健康SD大鼠静态吸入染毒,羰基镍低、中、高染毒浓度分别为20、135和250mg/m3,以氯气250mg/m3染毒为阳性对照组,均染毒30min,并设空白对照组。染毒后第1、2、3、7天取材,应用黄嘌呤氧化酶测定法分别测定各脏器中SOD活力。结果低、中浓度羰基镍染毒组心、脾、肾组织中SOD活力低于空白对照组,但差异无统计学意义(P>0.05),高浓度羰基镍组明显抑制SOD活力(P<0.05)。抑制作用以染毒后第3天最重(P<0.05),第7天时渐恢复,与阳性对照组比较,差异无统计学意义(P>0.05)。氯气染毒组心、脾组织中SOD活力抑制程度高于羰基镍染毒组,但高浓度羰基镍染毒组肾组织中SOD活力低于空白对照组。结论吸入羰基镍可致心、脾、肾组织中SOD活力不同程度的下降,诱发组织氧化损伤。
OBJECTIVE: To investigate the dynamic changes of superoxide dismutase (SOD) activity in heart, spleen and kidney of rats exposed to carbonyl nickel and compare the changes of SOD activity in different organs to explore the acute toxicity of nickel carbonyl. Methods Healthy SD rats were exposed to static inhalation. The concentration of carbonyl nickel was 20,135 and 250 mg / m3, and the concentrations of nickel carbonyl were 20, 135 and 250 mg / m3, respectively. All the rats were exposed to chlorine 250 mg / m3 for 30 min. Control group. 1, 2, 3 and 7 days after exposure, the activities of SOD in various organs were determined by xanthine oxidase assay. Results The activity of SOD in the heart, spleen and kidney tissues of low and medium concentration carbonyl nickel exposure groups was lower than that of the blank control group, but the difference was not statistically significant (P> 0.05). The high concentration carbonyl nickel group significantly inhibited the SOD activity (P <0.05 ). The inhibitory effect was the heaviest on day 3 (P <0.05) and gradually recovered on the 7th day. There was no significant difference between the control group and the positive control group (P> 0.05). The inhibition of SOD activity in heart and spleen of chlorine-exposed group was higher than that of carbonyl nickel-exposed group, but the activity of SOD in renal tissue of high-concentration carbonyl nickel-exposed group was lower than that of blank control group. Conclusion Inhalation of carbonyl nickel can cause SOD activity in heart, spleen and kidney to decrease to different extents, inducing tissue oxidative damage.