期刊论文

中文

环境与健康杂志

1001-5914

2003

20

2

81-83

10.16241/j.cnki.1001-5914.2003.02.006

国家科技攻关项目

本校为第一机构

目的探讨经不同浓度气态甲醛暴露的小鼠,不同组织器官的氧化损伤作用及其分子机理.方法用不同剂量气态甲醛对小鼠进行染毒处理72 h,测定吸入甲醛后5种脏器(脑、心、肺、肝、肾)超氧化物歧化酶(SOD)的水平.结果吸入1.2 mg/m3甲醛的小鼠,肝脏组织的SOD活性显著下降(P＜0.01);吸入3.7 mg/m3甲醛的小鼠,肝脏、肾脏、肺组织的SOD活性均显著下降(P＜0.001,P＜0.01,P＜0.05),其中对肝脏组织SOD的抑制作用尤为明显.结论气态甲醛对机体组织器官有氧化损伤作用,其分子机理涉及对SOD的抑制作用.

Objective To study the oxidation damage effects of gaseous formaldehyde on organs of mice and the moleculor mechanisms of the effects. Methods The mice were treated by different doses of gaseous formaldehyde (1.2 mg/m3 and 3.7 mg/m3) via inhalation for 72 hours, and the superoxide dismutase (SOD) activities of 5 organs (brain, lung, heart, liver, and kidney) were measured. Results The SOD activity in the liver decreased significantly (P