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Complex epigenetic patterns in cerebellum generated after developmental exposure to trichloroethylene and/or high fat diet in autoimmune-prone mice.
Environmental Science: Processes & Impacts ( IF 4.3 ) Pub Date : 2020-01-02 , DOI: 10.1039/c9em00514e Sarah J Blossom 1 , Stepan B Melnyk , Frank A Simmen
Environmental Science: Processes & Impacts ( IF 4.3 ) Pub Date : 2020-01-02 , DOI: 10.1039/c9em00514e Sarah J Blossom 1 , Stepan B Melnyk , Frank A Simmen
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Trichloroethylene (TCE) is an environmental contaminant associated with immune-mediated inflammatory disorders and neurotoxicity. Based on known negative effects of developmental overnutrition on neurodevelopment, we hypothesized that developmental exposure to high fat diet (HFD) consisting of 40% kcal fat would enhance neurotoxicity of low-level (6 μg per kg per day) TCE exposure in offspring over either stressor alone. Male offspring were evaluated at ∼6 weeks of age after exposure beginning 4 weeks preconception in the dams until weaning. TCE, whether used as a single exposure or together with HFD, appeared to be more robust than HFD alone in altering one-carbon metabolites involved in glutathione redox homeostasis and methylation capacity. In contrast, opposing effects of expression of key enzymes related to DNA methylation related to HFD and TCE exposure were observed. The mice generated unique patterns of anti-brain antibodies detected by western blotting attributable to both TCE and HFD. Taken together, developmental exposure to TCE and/or HFD appear to act in complex ways to alter brain biomarkers in offspring.
中文翻译：
自身免疫易发性小鼠发育暴露于三氯乙烯和/或高脂饮食后，在小脑中产生复杂的表观遗传模式。
三氯乙烯（TCE）是与免疫介导的炎性疾病和神经毒性相关的环境污染物。基于发育过度营养对神经发育的已知负面影响，我们假设发育暴露于高脂饮食（HFD）（由40％大卡脂肪组成）会增加后代中低水平（每公斤每天6μg）TCE暴露的神经毒性。单独的压力源。在母羊受孕前4周开始直至断奶，在暴露后约6周龄对雄性后代进行评估。无论是单次暴露还是与HFD一起使用，TCE在改变涉及谷胱甘肽氧化还原稳态和甲基化能力的一碳代谢物方面似乎都比单独使用HFD更为强大。相比之下，观察到与HFD和TCE暴露相关的DNA甲基化相关的关键酶表达的相反作用。小鼠产生了由TCE和HFD引起的Western印迹检测到的独特的抗脑抗体模式。两者合计，TCE和/或HFD的发育暴露似乎以复杂的方式起作用，以改变后代中的脑生物标志物。
更新日期：2020-03-27
中文翻译：
自身免疫易发性小鼠发育暴露于三氯乙烯和/或高脂饮食后，在小脑中产生复杂的表观遗传模式。
三氯乙烯（TCE）是与免疫介导的炎性疾病和神经毒性相关的环境污染物。基于发育过度营养对神经发育的已知负面影响，我们假设发育暴露于高脂饮食（HFD）（由40％大卡脂肪组成）会增加后代中低水平（每公斤每天6μg）TCE暴露的神经毒性。单独的压力源。在母羊受孕前4周开始直至断奶，在暴露后约6周龄对雄性后代进行评估。无论是单次暴露还是与HFD一起使用，TCE在改变涉及谷胱甘肽氧化还原稳态和甲基化能力的一碳代谢物方面似乎都比单独使用HFD更为强大。相比之下，观察到与HFD和TCE暴露相关的DNA甲基化相关的关键酶表达的相反作用。小鼠产生了由TCE和HFD引起的Western印迹检测到的独特的抗脑抗体模式。两者合计，TCE和/或HFD的发育暴露似乎以复杂的方式起作用，以改变后代中的脑生物标志物。
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