BPDE

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。

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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。

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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

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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。

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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。

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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。

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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。

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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。

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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。

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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

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