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[羰基镍急性中毒大鼠肺组织中Na(+)-K+ ATP酶活性及Na(+)-K+ ATP酶α1 mRNA表达的观察]

[Observation on both Na(+)-K+ Atpase activity and expression of Na(+)-K+ AtPase alpha1 mRNA in lung tissues of rats acute poisoned with nickel carbonyl].

作者信息

Shi Haiying, Wang Ning, Wang Qiuying, Pu Hongquan, Zhang Xiaopei, Shang Hui, Xuan Xiaoqiang, Ma Guoyu, Cheng Ning

机构信息

School of Public Health, Lanzhou University, Lanzhou 730000, China.

出版信息

Wei Sheng Yan Jiu. 2013 Sep;42(5):818-21.

Abstract

OBJECTIVE

To examine the change of Na(+)-K+ ATPase activity and the expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues of rats poisoned by nickel carbonyl and to discuss the mechanism of lung injury.

METHODS

One hundred seventy healthy rats (85 male and 85 female) were exposed by inhalation of 20,135 and 250 mg/m3 nickel carbonyl for 30 min. Rats poisoned by chlorine gas with a concentration 250 mg/m3 served as positive group and healthy SD rats served as no-treatment negative group. The rats were euthanized on 1, 2, 3 and 7 d after the administration of nickel carbonyl or chlorine gas. In various treatment groups, Na(+)-K+ ATPase activity was studied by colorimetric method and the expressions of Na(+)-K+ ATPase alpha1 mRNA were determined by RT-PCR.

RESULTS

Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues decreased in all treatment groups and chlorine gas-poisoned group, especially it was obvious decreased on the 2ed and 3rd day (P < 0.05).

CONCLUSION

Nickel carbonyl could induce lung damage and decrease Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung.

摘要

目的

观察羰基镍中毒大鼠肺组织钠钾ATP酶(Na(+)-K+ ATPase)活性及钠钾ATP酶α1亚基(Na(+)-K+ ATPase alpha1)mRNA表达变化,探讨羰基镍肺损伤机制。

方法

将170只健康大鼠(雌雄各85只),分别吸入20、135和250 mg/m3羰基镍30分钟染毒,以250 mg/m3氯气中毒大鼠为阳性对照组,健康SD大鼠为未处理阴性对照组。于染毒后1、2、3和7天处死大鼠,采用比色法检测各处理组大鼠肺组织Na(+)-K+ ATPase活性,逆转录聚合酶链反应(RT-PCR)法检测Na(+)-K+ ATPase alpha1 mRNA表达。

结果

各染毒组及氯气中毒组大鼠肺组织Na(+)-K+ ATPase活性及Na(+)-K+ ATPase alpha1 mRNA表达均降低,以染毒后第2、3天降低明显(P < 0.05)。

结论

羰基镍可致大鼠肺损伤,引起肺组织Na(+)-K+ ATPase活性及Na(+)-K+ ATPase alpha1 mRNA表达降低。

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