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首页> 外文期刊>Scientific reports. >Effects of first-generation in utero exposure to diesel engine exhaust on second-generation placental function, fatty acid profiles and foetal metabolism in rabbits: preliminary results
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Effects of first-generation in utero exposure to diesel engine exhaust on second-generation placental function, fatty acid profiles and foetal metabolism in rabbits: preliminary results

机译：兔子二代胎盘功能，脂肪酸谱和胎儿代谢在兔子柴油机排气中的第一代在兔子中的影响：初步结果

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Atmospheric pollution has major health effects on directly exposed subjects but intergenerational consequences are poorly characterized. We previously reported that diesel engine exhaust (DE) could lead to structural changes in the placenta of in utero exposed rabbits (first generation, F1). The effects of maternal exposure to DE were further studied on second-generation (F2) rabbits. Pregnant F0 females were exposed to filtered, diluted DE (1?mg/msup3/sup, median particle diameter: 69?nm) or clean filtered air (controls) for 2?h/day, 5 days/week by nose-only exposure during days 3-27 post-conception (dpc). Adult female offspring (F1) were mated to control males: F1 tissues and F2 foeto-placental units were collected at 28 dpc and placental structure and gene expression (microarray) analysed. Fatty acid profiles were determined in foetal and maternal plasma, maternal liver and placenta. In F1, compared to controls, hepatic neutral lipid contents were increased in exposed animals without change in the blood biochemistry. In F2, the placental lipid contents were higher, with higher monounsaturated fatty acids and reduced pro-inflammatory arachidonic acid (AA), without placental structural changes. Conversely, the proportion of anti-inflammatory n-3 polyunsaturated fatty acids in F2 plasma was increased while that of AA was decreased. Gene set enrichment analyses (GSEA) of F2 placenta transcriptomic data identified that the proteasome complex and ubiquitin pathways genes were over-represented and ion channel function and inflammation pathways genes were under-represented in exposed animals. These preliminary results demonstrate that diesel engine exhaust exposure and in utero indirect exposure should be considered as a programming factor within the context of the DOHaD (Developmental Origins of Health and Disease) with a probable intergenerational transmission.
机译：大气污染对直接暴露的受试者具有重大的健康影响，但代际后果表现不佳。我们之前报道，柴油发动机排气（DE）可能导致UTERO暴露的兔子的胎盘结构变化（第一代，F1）。在第二代（F2）兔中进一步研究了母体暴露于DE的影响。将怀孕的F0雌性暴露过滤，稀释的de（1？mg / m 3 ，中值粒径：69〜nm）或干净的过滤空气（对照）2〜h /天，5天/在概念后3-27天仅鼻子曝光的一周（DPC）。成年女性后代（F1）被配合以控制男性：在28dpc和胎盘结构和基因表达（微阵列）下收集F1组织和F2 FOETO-胎盘单元。在胎儿和母体血浆，母体肝脏和胎盘中测定脂肪酸型材。在F1中，与对照相比，在暴露的动物中增加了肝中性脂质含量，而不会发生血液生物化学。在F2中，胎盘脂质含量较高，具有较高的单一饱和脂肪酸和减少的促炎疟原虫（AA），没有胎盘结构变化。相反，抗炎N-3多不饱和脂肪酸在F2等离子体中的比例增加，而AA的抗炎脂肪酸增加。 F2胎盘转录组数据的基因设定富集分析（GSEA）确定了蛋白酶体复合物和遍难素途径基因被过度代表，并且在暴露的动物中欠离子通道功能和炎症途径基因。这些初步结果表明，柴油发动机排气暴露和在子宫间接曝光中应被视为具有可能的代际透射的杜哈德（健康和疾病的发育起源）的上下文中的编程因素。

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