在2009—2010年南半球夏季,用大流量采样器(high-volume air sampler,HVAS)和聚胺酯泡沫(polyurethane foam,PUF)被动采样器采集了南极菲尔德斯半岛和阿德利岛6个点的大气样品,分析了HBCDs的浓度水平、异构体组成、气相-颗粒相分配和空...在2009—2010年南半球夏季,用大流量采样器(high-volume air sampler,HVAS)和聚胺酯泡沫(polyurethane foam,PUF)被动采样器采集了南极菲尔德斯半岛和阿德利岛6个点的大气样品,分析了HBCDs的浓度水平、异构体组成、气相-颗粒相分配和空间分布趋势.主动和被动采集大气样品中ΣHBCDs浓度(α-HBCD、β-HBCD、γ-HBCD的浓度)范围分别为n.d.(未检出)—2.73 pg·m^(−3)和0.41—3.39 pg·m^(−3),与北极和偏远地区浓度水平一致,远低于城市和工业区的污染水平.HBCDs在主动采集的颗粒相和气相中的平均比例分别为67%和33%,颗粒相以α-HBCD(57%)为主,气相以γ-HBCD(53%)为主;被动采集的PUF样品中γ-HBCD(64%)占优势.经过主动采样和被动采样的对比研究,对采样速率进行校正后,PUF被动采样器可以用于南极大气样品的采集.南极大气中HBCDs的检出,表明HBCDs具有持久性和潜在的长距离大气传输能力;南极长城站附近大气中HBCDs浓度水平略高,反映了有限的人类活动对南极环境产生了影响.展开更多
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/...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.展开更多
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)
文摘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.
