光气致小鼠肺脏细胞DNA损伤和凋亡

DNA damage and apoptosis of lung cells induced by phosgene in mice

目的研究光气致BALB/c小鼠肺水肿模型的肺脏的DNA损伤和凋亡。方法26只二级BALB/C小鼠,雄性,随机分为正常对照组和染毒组,各13只。正常对照组小鼠给予空气,染毒组小鼠给予11·9mg/L剂量的光气,时间均为5min,染毒后4h,比较2组小鼠肺脏的湿干比、病理学变化,单细胞凝胶电泳测定2组肺Ⅱ型细胞DNA损伤情况及对小鼠肺脏进行DNA琼脂糖凝胶电泳。结果11·9mg/L的光气染毒5min,小鼠肺脏湿干比(6·42±1·00)比正常对照组(4·25±0·47)显著增加(P<0·05);光镜下观察肺组织可见肺水肿发生;单细胞凝胶电泳法测定染毒组肺Ⅱ型细胞的尾长、尾部DNA、尾距均显著高于正常对照组(P<0·001);DNA琼脂糖凝胶电泳出现DNA梯状样改变。结论光气染毒可造成小鼠肺水肿,引起肺Ⅱ型细胞发生DNA损伤和肺脏细胞凋亡。

Objective To study formation of pulmonary edema, DNA damage and apoptosis of lung cells induced by phosgene in BALB/C mice. Methods 26 mice were randomly divided into negative group and positive group, 13 mice in each. Mice were exposed to air or phosgene for 5 min in negative and positive group respectively. Dose of phosgene was 11.9mg/L. After exposed to phosgene for 4 h, all mice were anesthetized and removed for determination lung wet/dry weight ratio, alternation of lung tissue in optical microscope, DNA damage of alveolus type Ⅱ cells by single ceil gel electrophoresis and apoptosis of lung cells. Results After exposed, lung wet/dry weight ratio was significantly higher in mice for phosgene vs air（P〈0.05）. Lung visual field under microscope showed edema-like changes. The tail lengths, percentage of tail DNA and tail moment significantly increased in alveolus type Ⅱ cells of positive group compared with that of negative group. Signs of DNA laddering were observed in lung tissue of positive group. Conclusion Phosgene could cause pulmonary edema in mice, and could induce DNA damage and apoptosis of lung cells.