DNA adducts and P450 induction in human, rat and avian liver cells after exposure to polychlorobiphenyls
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Cited by (37)
Bacterial mutagenicity of selected procarcinogens in the presence of recombinant human or rat cytochrome P4501A1
2018, Mutation Research - Genetic Toxicology and Environmental MutagenesisPolychlorinated biphenyl quinone-induced genotoxicity, oxidative DNA damage and γ-H2AX formation in HepG2 cells
2014, Chemico-Biological InteractionsDNA double-strand breaks in relation to persistent organic pollutants in a fasting seabird
2014, Ecotoxicology and Environmental SafetyCitation Excerpt :If not repaired, DSBs may result in loss of chromosomes and/or cell death, mutations, chromosomal rearrangements (Thacker, 1986; Jackson, 1999) and carcinogenesis (Jeggo, 1998; Kanaar et al., 1998; Pfeiffer, 1998). Dubois et al. (1995) have shown that, when exposed in vitro, PCBs caused genotoxic effects on avian cells. Also, gel electrophoresis has been applied to study DSBs after genotoxic exposure in glaucous gulls (Larus hyperboreus) (Krøkje et al., 2006) and in fish blood cells (Theodorakis et al., 1994).
Polychlorinated biphenyls (PCBs) as initiating agents in hepatocellular carcinoma
2013, Cancer LettersCitation Excerpt :Most of the compound was bound to nuclear protein, only a very small amount of the photo-induced adducts was associated with purine nucleotides. In 1995 it was reported that after exposure of primary fetal rat and quail egg hepatocytes and human HepG2 hepatoma cells to 3,3′,4,4′-tetrachlorobiphenyl (PCB77), a significant level of DNA adducts was seen, i.e. 37 with quail and 20 adducts per 109 nucleotides with the rat and human cells [18]. Interestingly, the level of EROD (CYP1A1) activity did not correlate with the level of adduct formation, suggesting that other CYPs may have been involved in the bioactivation of PCB77.
Mutagenicity of 3-methylcholanthrene, PCB3, and 4-OH-PCB3 in the lung of transgenic BigBlue<sup>®</sup> rats
2008, Environmental Toxicology and PharmacologyCitation Excerpt :Indeed, a study examining retention of PCBs in rats after oral application found hydroxylated PCB metabolites in both, the lungs and livers (Bergman et al., 1994). Such activated biphenyls may result in the formation of DNA adducts and subsequently DNA damage (Dubois et al., 1995; Wong et al., 1979), a mechanism that could result in cancer initiation. In rodents the most common tumor site after PCB-exposure is the liver (Mayes et al., 1998), but lung tumors were also described after exposure to PCB mixtures (Anderson et al., 1994; Nakanishi and Shigematsu, 1991) or individual PCB congeners (NTP, 2006a,b).