摘要
目的探索气态甲醛暴露对小鼠肺组织一氧化氮(NO)代谢的影响。方法24只成年雄性昆明小鼠随机分4组,每组6只,连续72h用不同浓度气态甲醛(0、0.5、1.0、3.0mg/m3)对小鼠进行仿真式染毒,测定小鼠肺组织中一氧化氮合酶(NOS)活力水平和NO阳性检出率。结果低浓度甲醛暴露(≤0.5mg/m3)可抑制肺组织NOS活力(P<0.05),NO浓度很低,而高浓度甲醛暴露则可使肺组织NOS水平升高(P<0.05),气道的NO浓度增高。结论甲醛在机体内存在双向作用,随着甲醛浓度升高,小鼠肺组织NOS活力呈现先抑制而后升高的变化趋势,其NO阳性检出率亦呈现此规律。
Objective To study the impact of gaseous formaldehyde exposure on the metabolism of nitric oxide (NO) in the lung tissue of mice. Methods The adult male Kunming mice were randomly divided into 4 groups, treated with gaseous formaldehyde (0,0.5,1,3 mg/m3) for consecutive 72 h in the simulated exposure chamber, the nitric oxide synthase (NOS) activities and the NO positive rate in mice's lung were measured with the reagent kits. Results The lower formaldehyde exposure (≤0.5 mg/m3 ) could decrease NOS activity (compared with the control, P<0.05) and make NO hardly be determined, otherwise the high formaldehyde exposure could significantly increase NOS activity (compared with the control, P<0.05) and make NO increasing as well. Conclusion We consider that formaldehyde will play a double role in vivo, that is, low formaldehyde exposure may decrease NOS activities and NO, therefore asthma will not occur in the one hand, the NOS activities will be stimulated and the NO concentration in the airways will be increased by a high formaldehyde exposure, as a result, asthma will occur in the other hand.
出处
《环境与健康杂志》
CAS
CSCD
北大核心
2004年第6期368-370,共3页
Journal of Environment and Health
基金
国家"十五"科技攻关课题(2001BA704B01)
关键词
甲醛
一氧化氮合酶
一氧化氮
哮喘
Formaldehyde
Nitric oxide synthase
Nitric oxide
Asthma
