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Ji, Kyunghee,Choi, Kyungho,Giesy, John P.,Musarrat, Javed,Takeda, Shunichi American Chemical Society 2011 Environmental science & technology Vol.45 No.11
<P>Polybrominated diphenyl ethers (PBDEs) have been extensively utilized as flame retardants, and recently there has been concern about potential adverse effects in humans and wildlife. Their hydroxylated analogs (OH-BDEs) have received increasing attention due to their potential for endocrine and neurological toxicities. However, the potentials and mechanisms of genotoxicity of these brominated compounds have scarcely been investigated. In the present study, genotoxicity of tetra-BDEs, penta BDE, octa-BDE, deca-BDE, and tetra-OH-BDEs were investigated by use of chicken DT40 cell lines including wild-type cells and a panel of mutant cell lines deficient in DNA repair pathways. Tetra-BDEs have greater genotoxic potential than do the other BDEs tested. OH-tetra-BDEs were more genotoxic than tetra-BDEs. DT40 cells, deficient in base excision repair (<I>Pol</I>β<SUP>–/–</SUP>) and translesion DNA synthesis (<I>REV3</I><SUP>–/–</SUP>) pathways, were hypersensitive to the genotoxic effects of tetra-BDEs and OH-tetra-BDEs. The observation of chromosomal aberrations and gamma-H2AX assay confirmed that the studied brominated compounds caused double strand breaks. Pretreatment with <I>N</I>-acetyl-<SMALL>l</SMALL>-cysteine (NAC) significantly rescued the <I>Pol</I>β<SUP>–/–</SUP> and <I>REV3</I><SUP>–/–</SUP> mutants, which is consistent with the hypothesis that PBDEs and OH-BDEs cause DNA damage mediated through reactive oxygen species (ROS). Some tetra-BDEs and OH-tetra-BDEs caused base damage through ROS leading to replication blockage and subsequent chromosomal breaks.</P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/es104344e'>ACS Electronic Supporting Info</A></P>
Ji, Kyunghee,Seo, Jihyeon,Liu, Xiaoshan,Lee, Jinyoung,Lee, Sangwoo,Lee, Woojin,Park, Jeongim,Khim, Jong Seong,Hong, Seongjin,Choi, Yeyong,Shim, Won Joon,Takeda, Shunichi,Giesy, John P.,Choi, Kyungho American Chemical Society 2011 Environmental science & technology Vol.45 No.17
<P>The <I>Hebei Spirit</I> oil spill episode (December 7, 2007) has affected the western coastal area of South Korea; however, there is limited information on the potential toxicity of the oil spill to the ecosystem or humans. The potential toxicity of sediments collected from the affected area (<I>n</I> = 22) 2 years after the spill was evaluated. Acute lethal toxicity tests using <I>Vibrio fischeri</I> and <I>Moina macrocopa</I> and tests for genotoxicity and alteration of steroidogenesis using chicken DT40 cells and H295R cells, respectively, were conducted. Both crude and weathered oil extracts were evaluated in order to link the observed toxicity in the sediment extracts to the oil spill. Whereas toxicity to bacteria and daphnids was observed in only two elutriate samples, 10 of the 22 sediment extracts showed genotoxic potential in DT40 cells. The mechanisms of genotoxicity involved nucleotide excision repair (XPA<SUP>–/</SUP>), homologous recombination (RAD54<SUP>–/–</SUP>), and translesion synthesis pathways (REV3<SUP>–/–</SUP>). In addition, nine sediment extracts caused significantly greater production of E2 in H295R cells, and significant up-regulation of CYP19, CYP11B2, and 3βHSD2 by sediment extracts was observed. The pattern of toxicities observed in both crude and weathered oil samples was similar to that observed in the sediment extracts. The genotoxicicity and endocrine-disruption potential of the sediment extracts suggest a need for long-term followup for such toxicity in humans and wildlife in this area.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/esthag/2011/esthag.2011.45.issue-17/es200724x/production/images/medium/es-2011-00724x_0003.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/es200724x'>ACS Electronic Supporting Info</A></P>