The cytotoxic effect of polycyclic aromatic hydrocarbons in oral and bronchial epithelial cells

• Main Authors: Tan-Yu Hsu, 許瑭裕
• Other Authors: Chang-Shen Lin
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/76342888173041860174

碩士 === 高雄醫學大學 === 醫學研究所 === 96 === Abstract Polycyclic aromatic hydrocarbons (PAHs) are a large group of organic compounds composing of two or more fused aromatic rings. Probably have more than 1000 kinds. They are produced by cigarette smoking and by any type of incomplete combustion. PAHs may be carcinogenic to human. Their metabolites may form adducts with DNA and may induce DNA damage. To examine the roles of PAHs in contributing cigarette smoking-associated human malignancies, we investigate cytotoxicity and genotoxicity of various PAHs in oral (KB) and bronchial epithelial (Beas-2B) cell lines. The 9 PAHs with potential carcinogenicity announced by the United State Environmental Protection Agency were used in this study. By MTT assays done after PAHs treatment for 24 hr, we found that BaA, BaP, and FL-treated cells exhibited growth advantage in Beas-2B but not in KB cells. However, the cell growth was repressed in both cell lines when they were incubated with PAHs for one week or longer periods. Flow cytometric analyses showed that BaP treatment for 24 hr could increase S phase propotion in KB but not in Beas-2B cells. When Beas-2B cells were incubated with BaP for 7 days, most cells were arrested in G2/M phase. To examine whether the cytotoxicity of BaP was correlated to BaP-associated DNA damage and repair, we conducted host cell reactivation assays, which could evaluate nucleotide excision repair (NER). The results showed that BaP could inhibit NER both in KB and in Beas-2B cells. Besides, we found that micronucleus formation was increased in BaP-treated KB and Beas-2B cells. These results suggested that BaP could repress DNA repair and induce sign of genomic instability.