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作 者:LI Rui Jing GAO Hui NA Guang Shui LU Zi Hao YAO Yao YANG Fan
机构地区:[1]Key Laboratory for Ecological Environment in Coastal Areas,National Marine Environmental Monitoring Center Dalian 116023,Liaoning,China [2]Shanghai Ocean University,Shanghai 201306,China
出 处:《Biomedical and Environmental Sciences》2017年第4期296-300,共5页生物医学与环境科学(英文版)
基 金:supported by the National Natural Science Foundation of China(No.41406088);The open fund of Key Laboratory for Ecological Environment in Coastal Areas,State Oceanic Administration(201506)
摘 要:To investigate the genotoxicity and reveal the potential toxicological mechanisms of Hexabromocyclododecane (HBCD), human breast cells HBL-100 were exposed to a sequence of HBCD concentrations (0, 5, 10, and 50 mg/L) for 24 h. With a series of zymology and molecular biology methods, we found that HBCD induced dose-dependent oxidative stress on HBL-100 DNA. As revealed in q RT-PCR, activated prognostic factor ATM down-regulated tumor suppressor gene BRCA1 and prompted DNA repair genes h OGG1 and h MTH1 expression in lower concentrations of HBCD (〈 10 mg/L). However, DNA repair were inhibited as well as cell proliferation rate by higher concentrations of HBCD (50 mg/L). The results inferred that the genotoxicity of HBCD was dose-dependent and related to DNA repair pathway.To investigate the genotoxicity and reveal the potential toxicological mechanisms of Hexabromocyclododecane (HBCD), human breast cells HBL-100 were exposed to a sequence of HBCD concentrations (0, 5, 10, and 50 mg/L) for 24 h. With a series of zymology and molecular biology methods, we found that HBCD induced dose-dependent oxidative stress on HBL-100 DNA. As revealed in q RT-PCR, activated prognostic factor ATM down-regulated tumor suppressor gene BRCA1 and prompted DNA repair genes h OGG1 and h MTH1 expression in lower concentrations of HBCD (〈 10 mg/L). However, DNA repair were inhibited as well as cell proliferation rate by higher concentrations of HBCD (50 mg/L). The results inferred that the genotoxicity of HBCD was dose-dependent and related to DNA repair pathway.
关 键 词:DNA HBCD Hexabromocyclododecane-induced Genotoxicity in Cultured Human Breast Cells through DNA Damage
分 类 号:R114[医药卫生—卫生毒理学]
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