BPDE

The changes of 8-OH-dG in the progress of carcinogenesis were detected in human bronchial epithelial cells induced by Benzo ( a) pyrene diol-epoxide ( BPDE) and sulfide nickel ( NiS) in vitro.

并利用苯并（a）芘代谢产物B（a）P二醇环氧化物（BPDE）和结晶型硫化镍（NiS）诱导的体外人支气管上皮细胞转化癌变模型，检测癌变进程中8OH dG的变化。

Mutation induced by ￣( 60) Co γ-ray BPDE in msu-1 · 1 human fibroblast at the HPRT locus

~（60）Coγ射线和BPDE诱发人成纤维细胞hprt基因突变的研究

BPDE-DNA adducts in white blood cell could be used as effect biomarker of DNA damage in population by PM2.5 without special exposure to PAHs.

若无特殊PAHs暴露，可将外周血白细胞BPDE-DNA加合物作为PM2.5致人群DNA损伤的效应生物标志。

Conclusions Anti-BPDE can result in DNA strand breakage, and the degrees of damage is related to the administrated doses of anti BPDE.

结论反式BPDE可导致DNA断裂损伤，其损伤程度与剂量有一定关系。

The tumor was squamose carcinoma confirmed by histopathological examination. The culture system in this study provided a potential tool for studying the molecular mechanism of carcinogenesis of human bronchial epithelial cells induced by BPDE.

本实验以反式BPDE成功地诱发了人支气管上皮细胞恶性转化，为后期进一步研究其致癌的分子机制、寻找致癌相关基因提供了理想的生物学材料。

Full-length Cloning of brg, the Anti-BPDE Related Gene

反式二羟环氧苯并（a）芘相关新基因brg的全长克隆

The content increase of 8-OH-dG was in accordance with the progress of cell carcinogenesis, which was displayed in human bronchial epithelial cells induced by BPDE and NiS.

在体外用BPDE和NiS作用于人支气管上皮细胞系诱导其转化和癌变过程中，8OH dG出现于细胞转化之前，其含量的增加与细胞癌变进程相一致。

A comparative study on mutation by γ-radiation and BPDE was conducted in MSU-1 · 1 human fibroblasts at the hprt gene.

对γ射线和BPDE诱发人成纤维细胞株MSU－1·1bprt基因突变进行了比较研究。

Methods A549 cells cultured in vitro were divided into heat stress group and BPDE group.

方法体外培养的A549细胞分为高温应激组和BPDE组。

Objective The carcinogenesis mechanism of benzo [ α] pyrene dihydrodiol epoxide ( BPDE) is still unclear according to the known genes interaction with BPDE. So it is an urgent problem to screen more BPDE target susceptible genes.

研究目的：目前已知的与二羟环氧苯并芘（BPDE）相互作用的基因尚不能阐明BPDE的致癌分子机制，寻找出更多的BPDE致癌易感基因是个亟需解决的问题。