膜脂过氧化产物在光敏诱发细胞突变中的作用  

Role of lipid peroxidation products in cell mutagenesis induced by photosensitization

作　　者：曹恩华[1] 许娜飞[1] 张健[1] 李景福[1] 王菊君 

机构地区：[1]中国科学院生物物理研究所

出　　处：《激光生物学报》1998年第1期3-7,共5页Acta Laser Biology Sinica

基　　金：国家自然科学基金

摘　　要：本文选用ＣＨＯ细胞，通过竹红菌甲素（ＨＡ）光敏诱变及ｏｕａ选择性培养液的筛选，证实甲素光敏反应对细胞Ｎａ＋／Ｋ＋ＡＴＰ酶基因具有诱变致突作用。对其突变效应与脂质过氧化反应及ＤＮＡ加成物形成关系的分析表明，ＴＢＡ反应产物随着光照时间的增加而增加，同时ＤＮＡ加成物生成迅速增加，突变频率也随之增高。维生素Ｅ可抑制脂质过氧化反应，并减少ＤＮＡ加成物生成，阻止细胞突变率的增加。提示光敏诱发细胞脂质过氧化所产生的活性产物可能是造成细胞基因突变的重要原因之一。In the present study, the mutation effects of Hypocrellin A on CHO cell were investigated by analysis of the mutant defection in Na +/K + ATPase gene induced by HA photosensitization and then selected by ouabain. The result shows that HA photosensitization has the ability to cause cell DNA point mutation. Further the analysis of relation among the cell mutation frequencies, lipid peroxidation degree and lipidDNA adduct formation in cells labeled with arachidonic acid and exposed to HA plus light shows that TBA reaction products increased with increase of irradiation time, lipidDNA adduct formation and cell mutation frequencies increased in the meantime. Addition of Vitamin E inhibited the lipid peroxidation, lipidDNA adduct formation and cell mutation frequencies decreased in the meantime. Above results suggest that the lipid peroxidation by HA photosensitization plays an important role in the cell DNA damage and gene mutation.

关 键 词：竹红菌甲素 光敏反应 脂质过氧化 基因突变 

分 类 号：Q343.13[生物学—遗传学] Q63