吸入甲醛对小鼠肺脏的损伤

Lung Injury induced by Formaldehyde Inhalation in Mice

目的探讨甲醛中毒的肺脏损害机制。方法选择健康昆明小鼠40只,随机分为4组:甲醛低剂量组(2.5mg/m3)、中剂量组(5mg/m3)、高剂量组(10mg/m3)、阴性对照组,每组10只。除阴性对照组外,其余3个剂量组每日吸入甲醛1次,每次4h,连续9周。测定小鼠血浆、肺脏超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及小鼠肺脏谷胱甘肽过氧化物酶(GSH-Px)活性。结果高剂量染毒组小鼠血浆和中、高剂量染毒组小鼠肺脏MDA含量显著高于对照组(P<0.05或P<0.01);在所有染毒组肺和血浆SOD活力均低于对照组(P<0.05或P<0.01);中、高剂量染毒组肺GSH-Px活力低于低剂量组和阴性对照组(P<0.01)。结论吸入甲醛可引起小鼠肺组织发生氧化性损伤。

Objective To explore the mechanism of formaldehyde（FA） inhalation induced lung injury. Methods Forty healthy KM mice were randomly divided into 4 groups, and 10 mice in each group： FA low dose group（2.5mg/m^3 ）, FA middle- dose group（5mg/m^3 ）. FA high dose group（ 10mg/m^3 ）. and negative control group. Except the control group, the animals of the 3 experimental groups inhaled FA for 4h daily for 9 successive weeks. After exposure, the lung tissue and plasma malondialdehyde（MDA） levels and lung tissue superoxide dismutase（SOD） activity and glutathione peroxidase（GSH-Px） activity were examined. Results Compared with the control group, the MDA contents increased remarkably in lung tissue of both middle and high does groups, but increased only in plasma of high dose group（ P〈0.05 or P〈0.01 ）. The lung and plasma SOD activity were significantly declined in all of the experimental groups（ P 〈 0.05 or P 〈 0.01 ）. The GSH Px activity was significantly declined in lung tissue of both middle and high dose groups（ P〈 0.01 ）. Conclusion： Inhalation of FA induces oxidative stress injury in mice lung.