Yin Guoying, Xia Liting, Hou Yaxing, Li Yaoyan, Cao Deqing, Liu Yanan, Chen Jingshan, Liu Juan, Zhang Liwen, Yang Qiaoyun, Zhang Qiang, Tang Naijun
Department of Occupational and Environmental Health, School of Public Health, Tianjin Medical University, Tianjin, China.
Central Laboratory of Preventive Medicine, School of Public Health, Tianjin Medical University, Tianjin, China.
Int J Environ Health Res. 2022 Jun;32(6):1248-1260. doi: 10.1080/09603123.2020.1870668. Epub 2021 Jan 7.
Developmental exposure to environmental toxicants can induce transgenerational reproductive disease phenotypes through epigenetic mechanisms. We treated pregnant CD-1 (F0) mice with drinking water containing sodium arsenite (85 ppm) from days 8 to 18 of gestation. Male offspring were bred with untreated female mice until the F3 generation was produced. Our results revealed that F0 transient exposure to arsenic can cause decreased sperm quality and histological abnormalities in the F1 and F3. The overall methylation status of DMR2 and DMR was significantly lower in the arsenic-exposed group than that of the control group in both F1 and F3. The relative mRNA expression levels of and in arsenic-exposed males were significantly increased in both F1 and F3. This study indicates that ancestral exposure to arsenic may result in transgenerational inheritance of an impaired spermatogenesis phenotyping involving both epigenetic alterations and the abnormal expression of and .
发育过程中接触环境毒物可通过表观遗传机制诱发跨代生殖疾病表型。我们在妊娠第8天至18天用含亚砷酸钠（85 ppm）的饮用水处理怀孕的CD-1（F0）小鼠。雄性后代与未处理的雌性小鼠交配直至产生F3代。我们的结果显示，F0短暂接触砷可导致F1和F3的精子质量下降和组织学异常。在F1和F3中，砷暴露组的DMR2和DMR的总体甲基化状态均显著低于对照组。在F1和F3中，砷暴露雄性中相关基因的相对mRNA表达水平均显著增加。本研究表明，祖先接触砷可能导致精子发生受损表型的跨代遗传，这涉及表观遗传改变以及相关基因的异常表达。
