烹调油烟致肺损伤及可能机理的实验研究  

Experimental Study on Lesions and Its Machanisms of Lung in Rats Exposed to Cooking Oil Fumes

作　　者：让蔚清[1] 周少琴 苏琦[2] 李东阳 贺性鹏 谢红卫 

机构地区：[1]湖南省衡阳医学院卫生学教研室,衡阳市421001 [2]湖南省衡阳医学院肿瘤研究所

出　　处：《实用预防医学》2000年第2期96-97,共2页Practical Preventive Medicine

基　　金：湖南省教委资助!项目(编号 :97B0 98)

摘　　要：[目的 ]　探讨烹调油烟致肺损伤的可能机理。 [方法 ]　大鼠吸入浓度为 43± 4mg/m3 的烹调油烟 ,分三个时相观察肺部病理改变 ,肺S9中MDA含量及SOD酶活性 ,肺P53 基因表达蛋白水平。 [结果 ]　肺部病理改变以炎症为主 ,尚有肺泡上皮增生、腺样化生、不典型腺样增生。肺S9中MDA含量明显升高 ,SOD明显降低 ,增生肺组织中P53 蛋白表达增高。 [结论 ]　烹调油烟可致肺组织腺样化生与癌前病变 ,肺组织氧化损伤与P53 蛋白表达增高可能是肺部病变的机理。Objective] To observe pathological changes of lung tissues in rats exposed COF and reveal its machanisms. [Methods] SD rats inhaled COF (43±4 mg/m 3) to observe pathological changes of Lung tissues、 the concentration of malondiadehyde (MDA) and the activity of superoxide dismutase (SOD) in Lung S 9、the expression level of P 53 gene Protein. [Results] The main pathological changes of lung tissues are inflammation, alueder epithelial hyperplasia are also found. The concertration of MDA are significantly higher and the activity of SOD are lower than negative control group. The level of P 53 gene protein are higher. [Conclution] COF may cause adenic metaplasia and precancerous lesions. The oxidactive lesion and the mutation P 53 gene may be the mechanisms of pathological changes of lung tissues.

关 键 词：烹调油烟 病理改变 损伤机理 肺损伤 

分 类 号：R992[医药卫生—毒理学] R563[医药卫生—药学]