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 (PM_2.5) samples were collected in Taiyuan and pregnant rodent models were administered with 3 mg/kg b.w. PM_2.5 by 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 PM_2.5 exposure (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).

人体和动物实验的流行病学研究表明，妊娠暴露于大气污染物可能会导致胎盘发育异常。但是，这种暴露对胎盘营养运输的影响尚未得到系统的研究。在这项研究中，从太原采集了细颗粒物（PM _2.5）样品，从胚胎第0.5天（E0.5）开始，隔天通过口咽抽吸对怀孕的啮齿动物模型给予3 mg / kg bw PM _2.5。然后处死怀孕的小鼠，并在不同的时间点收集它们的胎盘。结果表明，孕妇PM _2.5暴露（MPE）在所有时间点都破坏了增殖细胞核抗原（PCNA）的表达，并抑制了胎盘中的细胞增殖。之后，胎盘营养运输的能力受到损害。在E18.5处的变化最明显，表明氨基酸，长链多不饱和脂肪酸（LCPUFA），葡萄糖和叶酸转运蛋白的mRNA表达改变。此外，MPE后胎盘中的糖原含量在E18.5升高，甘油三酸酯含量在E13.5和E15.5升高，在E18.5降低。简而言之，MPE引起的不良反应表明，MPE通过调节胎盘营养转运蛋白（PNT）的含量，导致发育中胎儿的营养供应中断。