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目的通过研究大鼠急性羰基镍中毒肝脏中钠钾ATP酶(Na+-K+ATPase)活力变化与钠钾ATP酶α1(Na+-K+ATPaseα1)基因表达,探讨急性羰基镍中毒对肝脏的急性毒性作用及其中毒机制。方法健康SPF级SD大鼠200只,分为5组,雌雄各半,静态吸入染毒,染毒时间为30min,羰基镍染毒浓度分别为20、135和250mg/m3,氯气染毒250mg/m3为阳性对照组,健康大鼠为正常对照组,染毒后第1、第2、第3和第7天分别取材,用定磷比色法测定Na+-K+ATP酶活力,用反转录-聚合酶链反应(RTPCR)方法测定Na+-K+ATPα1基因的表达水平。结果在低、中、高浓度羰基镍染毒条件下,肝脏中Na+-K+ATP酶活力均明显下降(P<0.05),以染毒第3天时肝脏中Na+-K+ATP酶降低最为明显(P<0.05);高浓度染毒组染毒第3天,肝脏中Na+-K+ATPα1基因表达低于对照组(P<0.05)。结论羰基镍可引起大鼠肝脏氧化损伤,明显降低Na+-K+ATP酶活力并影响α1基因表达。
OBJECTIVE: To investigate the changes of Na + -K + ATPase activity and Na + -K + ATPaseα1 gene expression in the liver of acute carbonyl nickel poisoning rats and to explore the acute liver toxicity caused by acute nickel carbonyl poisoning Role and poisoning mechanism. Methods 200 healthy SPF SD rats were randomly divided into 5 groups: male and female, inhaled by static inhalation, exposure time was 30 min, nickel carbonyl concentration was 20, 135 and 250 mg / m 3, chlorine exposure was 250 mg / m3 for the positive control group, healthy rats as a normal control group, 1, 2, 3 and 7 days after exposure were drawn, determined by fixed phosphorus colorimetric Na + -K + ATPase activity, with reversal The level of Na + -K + ATPα1 gene expression was determined by RTPCR. Results Under the condition of low, medium and high concentration of nickel carbonyl, the activity of Na + -K + ATPase in the liver decreased significantly (P <0.05), and the most obvious decrease of Na + -K + ATPase in the liver on the 3rd day (P <0.05). On the 3rd day after exposure, the expression of Na + -K + ATPα1 in the liver of the high concentration exposure group was lower than that of the control group (P <0.05). Conclusion Nickel carbonyl can cause oxidative damage in rat liver, significantly decrease the activity of Na + -K + ATPase and affect the expression of α1 gene.