Maternal PM2.5 exposure and abnormal placental nutrient transport
Maternal PM2.5 exposure and abnormal placental nutrient transport
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母体 PM2.5 暴露与胎盘营养转运异常
DOI：
10.1016/j.ecoenv.2020.111281
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发表时间：
2021
影响因子：
6.8
通讯作者：
Nan Sang
中科院分区：
文献类型：
--
作者：
Na Zhu;Xiaotong Ji;Xilin Geng;Huifeng Yue;Guangke Li;Nan Sang
人类和动物实验的流行病学研究表明，妊娠期暴露于大气污染物可能导致胎盘发育异常。然而，这种暴露对胎盘运输营养物质的影响还没有系统的研究。本研究在太原市采集细颗粒物（PM2.5）样本，从胚胎第0.5天（E0.5）开始，每隔一天通过口咽吸入3 mg/kg b.w的PM2.5。然后处死妊娠小鼠，在不同时间点采集胎盘。结果表明，母体pm2.5暴露（MPE）可在各时间点破坏增殖细胞核抗原（PCNA）的表达，抑制胎盘细胞增殖。随后，胎盘营养物质运输能力受损。在E18.5时变化最为显著，氨基酸、长链多不饱和脂肪酸（LCPUFA）、葡萄糖和叶酸转运蛋白mRNA表达发生改变。此外，MPE后胎盘中糖原含量在E18.5时升高，甘油三酯含量在E13.5和E15.5时升高，在E18.5时降低。总之，MPE的不良反应表明，MPE通过调节胎盘营养转运蛋白（PNT）的丰度，导致发育中的胎儿的营养供应中断。
Epidemiological studies of human and animal experiments indicated that gestational exposure to atmospheric pollutants could be followed by the abnormal placental development. However, the effects of this exposure on the placental transportation for nutrients have not been systematically investigated. In this study, fine particulate matters (PM2.5) samples were collected in Taiyuan and pregnant rodent models were administered with 3 mg/kg b.w. PM2.5by oropharyngeal aspiration every other day starting on embryonic day 0.5 (E0.5). Then the pregnant mice were sacrificed and their placentas were collected at different time points. The results showed that maternal PM2.5exposure (MPE) disrupted the expression of proliferating cell nuclear antigen (PCNA) at all time points and inhibited the cell proliferation in placenta. Following that, the capacity for placental nutrient transport was impaired. The changes at E18.5 were observed most significantly, showing the altered mRNA expression of amino acid, long-chain polyunsaturated fatty acid (LCPUFA), glucose and folate transporters. In addition, the glycogen content was elevated at E18.5, and the triglyceride content was increased at E13.5 and E15.5 and decreased at E18.5 in the placenta after MPE. In a word, the adverse effect induced by MPE revealed that MPE led tothe disruption on the nutrient supply to the developing fetus via modulating the abundance of placental nutrient transporters (PNT).