Sex-specific differences in genotoxic and epigenetic effects of 1,3-butadiene among mouse tissues
作者： Lauren Lewis , Grace A. Chappell , Tetyana Kobets , Bridget E. O’Brian , Dewakar Sangaraju
DOI: 10.1007/S00204-018-2374-X
关键词: DNA damage 、 Genotoxicity 、 Biology 、 DNA repair 、 DNA methylation 、 Epigenetics 、 Chromatin 、 Histone 、 Cancer research 、 Epigenome
摘要: Exposure to environmental chemicals has been shown have an impact on the epigenome. One example is a known human carcinogen 1,3-butadiene which acts primarily by genotoxic mechanism, but also disrupts chromatin structure altering patterns of cytosine DNA methylation and histone modifications. Sex-specific differences in 1,3-butadiene-induced genotoxicity carcinogenicity are well established; however, it remains unknown whether 1,3-butadiene-associated epigenetic alterations sex dependent. Therefore, we tested hypothesis that inhalational exposure will result sex-specific alterations. damage effects were evaluated liver, lung, kidney tissues male female mice two inbred strains (C57BL/6J CAST/EiJ). Mice exposed 0 or 425 ppm inhalation (6 h/day, 5 days/week) for 2 weeks. Strain- tissue-specific adducts crosslinks detected lung kidney; significant observed C57BL/6J only. In addition, assessed expression repair genes marked upregulation Mgmt mice. evident modifications liver both strains. Specifically, loss 1,3-butadiene-exposed mice, whereas hypermethylation was found CAST/EiJ Our findings suggest strain- epigenome may contribute cancer susceptibility.
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