Navasumrit Panida, Chaisatra Krittinee, Ruchirawat Mathuros
Rev Environ Health. 2016 Mar;31(1):11-2. doi: 10.1515/reveh-2015-0068.
Early life exposure to inorganic arsenic is associated with a wide range of malignant and chronic disease outcomes in humans. Prenatal arsenic exposure may give rise to adverse effects on child health and development as arsenic readily passes through the placenta in human beings. The impact of maternal arsenic exposure on fetal gene expression was conducted in pregnant women living in Southern Thailand. Arsenic exposed newborns had significantly higher levels of arsenic in cord blood, and a set of genes associated with numerous biological pathways, including cell signaling, apoptosis, inflammatory and stress response. A slight increase in promoter methylation of p53 in cord blood lymphocytes which correlated with arsenic accumulation in nails was observed in these exposed newborns. A follow-up study on these exposed children showed a significant increase in oxidative DNA damage, measured as 8-hydroxydeoxyguanosine (8-OHdG) in saliva. In addition, levels of urinary 8-OHdG excretion and salivary hOGG1 expression were significantly decreased in exposed children suggesting a defect in repair of 8-OHdG in arsenic-exposed children. Our study indicates that prenatal arsenic and continued exposure through early childhood can trigger various genetic and epigenetic alterations that may lead to disease development later in life.
早年接触无机砷与人类多种恶性和慢性疾病结局相关。由于砷在人体中很容易通过胎盘，产前接触砷可能会对儿童健康和发育产生不良影响。对生活在泰国南部的孕妇进行了母亲砷暴露对胎儿基因表达影响的研究。砷暴露的新生儿脐带血中的砷水平显著更高，并且有一组与众多生物途径相关的基因，包括细胞信号传导、细胞凋亡、炎症和应激反应。在这些暴露的新生儿中，观察到脐带血淋巴细胞中p53启动子甲基化略有增加，这与指甲中的砷积累相关。对这些暴露儿童的后续研究表明，以唾液中8-羟基脱氧鸟苷（8-OHdG）衡量的氧化DNA损伤显著增加。此外，暴露儿童的尿8-OHdG排泄水平和唾液hOGG1表达水平显著降低，表明砷暴露儿童的8-OHdG修复存在缺陷。我们的研究表明，产前砷暴露以及在幼儿期持续接触砷会引发各种基因和表观遗传改变，这些改变可能会导致日后疾病的发展。
