Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California 94720.
Colleges of Nanoscale Science and Engineering, State University of New York Polytechnic Institute, Albany, New York 12205.
Toxicol Sci. 2017 Nov 1;160(1):111-120. doi: 10.1093/toxsci/kfx159.
Trichloroethylene (TCE), an industrial chemical and environmental contaminant, is a human carcinogen. Reactive metabolites are implicated in renal carcinogenesis associated with TCE exposure, yet the toxicity mechanisms of these metabolites and their contribution to cancer and other adverse effects remain unclear. We employed an integrated functional genomics approach that combined functional profiling studies in yeast and avian DT40 cell models to provide new insights into the specific mechanisms contributing to toxicity associated with TCE metabolites. Genome-wide profiling studies in yeast identified the error-prone translesion synthesis (TLS) pathway as an import mechanism in response to TCE metabolites. The role of TLS DNA repair was further confirmed by functional profiling in DT40 avian cell lines, but also revealed that TLS and homologous recombination DNA repair likely play competing roles in cellular susceptibility to TCE metabolites in higher eukaryotes. These DNA repair pathways are highly conserved between yeast, DT40, and humans. We propose that in humans, mutagenic TLS is favored over homologous recombination repair in response to TCE metabolites. The results of these studies contribute to the body of evidence supporting a mutagenic mode of action for TCE-induced renal carcinogenesis mediated by reactive metabolites in humans. Our approach illustrates the potential for high-throughput in vitro functional profiling in yeast to elucidate toxicity pathways (molecular initiating events, key events) and candidate susceptibility genes for focused study.
三氯乙烯(TCE)是一种工业化学物质和环境污染物,也是一种人类致癌物。活性代谢物与 TCE 暴露相关的肾致癌作用有关,但这些代谢物的毒性机制及其对癌症和其他不良影响的贡献仍不清楚。我们采用了一种综合的功能基因组学方法,该方法结合了酵母和禽类 DT40 细胞模型中的功能谱研究,为深入了解与 TCE 代谢物相关的毒性的特定机制提供了新的见解。酵母中的全基因组谱研究确定易错跨损伤合成(TLS)途径是对 TCE 代谢物的重要反应机制。在 DT40 禽类细胞系中的功能谱研究进一步证实了 TLS DNA 修复的作用,但也揭示了 TLS 和同源重组 DNA 修复在高等真核生物对 TCE 代谢物的细胞易感性中可能发挥竞争作用。这些 DNA 修复途径在酵母、DT40 和人类之间高度保守。我们提出,在人类中,与同源重组修复相比,TCE 代谢物诱导的突变 TLS 更有利于突变。这些研究的结果为支持 TCE 诱导的肾致癌作用的反应性代谢物介导的致突变作用模式的证据体系做出了贡献。我们的方法说明了在酵母中进行高通量体外功能谱研究以阐明毒性途径(分子起始事件、关键事件)和候选易感性基因的潜力,以便进行重点研究。