Villarroel Francisca, Ramírez Eder, Ponce Nikol, Nualart Francisco, Salinas Paulo
Laboratory of Animal & Experimental Morphology, Institute of Biology, Faculty of Sciences, Pontificia Universidad Católica de Valparaíso, Valparaíso 2362807, Chile.
Laboratory of Neurobiology and Stem Cells NeuroCellT, Department of Cellular Biology, Faculty of Biological Sciences, Universidad de Concepción, Concepción 4070386, Chile.
Antioxidants (Basel). 2025 Aug 26;14(9):1050. doi: 10.3390/antiox14091050.
Fine particulate matter (PM2.5) emitted by wood smoke is a significant environmental pollutant associated with oxidative stress and hypoxia. These conditions can disrupt placental function by altering the expression of key nutrient transporters, such as glucose transporter 1 (GLUT1) and sodium-dependent vitamin C transporter 2 (SVCT2), which are essential for fetal development. This study evaluates the effects of pregestational and gestational exposure to PM2.5 on GLUT1 and SVCT2 expression in the rat placenta. Pregnant Sprague-Dawley rats were exposed to either filtered air (FA) or non-filtered air (NFA) containing PM2.5 from wood combustion in a controlled exposure system. Four experimental groups were established: FA/FA (control), FA/NFA (gestational exposure), NFA/FA (pregestational exposure), and NFA/NFA (continuous exposure). Immunofluorescence and confocal microscopy were used to quantify the expression of GLUT1 and SVCT2 in the placental labyrinth zone. Statistical analyses were performed using Kruskal-Wallis and post hoc Dunn's test ( < 0.05). Gestational exposure to PM2.5 (FA/NFA) significantly reduced GLUT1 and SVCT2 expression, compromising glucose transport and antioxidant protection in the placenta. Pregestational exposure (NFA/FA) induced a compensatory increase in SVCT2 expression, suggesting an adaptive response to oxidative stress. Continuous exposure (NFA/NFA) resulted in GLUT1 redistribution within the syncytiotrophoblast and decreased membrane localization, potentially impairing glucose uptake. PM2.5 exposure disrupts the expression and localization of GLUT1 and SVCT2 in the placenta, with differential effects depending on the timing of exposure. The gestational phase appears to be particularly vulnerable, as reduced GLUT1 and SVCT2 levels may impair fetal nutrition and antioxidant defense. These findings underscore the need for preventive measures to mitigate air pollution-related risks during pregnancy.
木烟排放的细颗粒物（PM2.5）是一种与氧化应激和缺氧相关的重要环境污染物。这些状况可通过改变关键营养转运蛋白的表达来破坏胎盘功能，例如对胎儿发育至关重要的葡萄糖转运蛋白1（GLUT1）和钠依赖性维生素C转运蛋白2（SVCT2）。本研究评估孕前和孕期暴露于PM2.5对大鼠胎盘GLUT1和SVCT2表达的影响。将怀孕的Sprague-Dawley大鼠在可控暴露系统中暴露于过滤空气（FA）或含有木燃烧产生的PM2.5的未过滤空气（NFA）中。设立了四个实验组：FA/FA（对照组）、FA/NFA（孕期暴露）、NFA/FA（孕前暴露）和NFA/NFA（持续暴露）。采用免疫荧光和共聚焦显微镜定量胎盘迷路区GLUT1和SVCT2的表达。使用Kruskal-Wallis检验和事后Dunn检验进行统计分析（<0.05）。孕期暴露于PM2.5（FA/NFA）显著降低了GLUT1和SVCT2的表达，损害了胎盘中的葡萄糖转运和抗氧化保护。孕前暴露（NFA/FA）诱导SVCT2表达代偿性增加，表明对氧化应激有适应性反应。持续暴露（NFA/NFA）导致GLUT1在合体滋养层内重新分布并减少膜定位，可能损害葡萄糖摄取。暴露于PM2.5会破坏胎盘中GLUT1和SVCT2的表达和定位，根据暴露时间不同产生不同影响。孕期似乎特别脆弱，因为GLUT1和SVCT2水平降低可能损害胎儿营养和抗氧化防御。这些发现强调了采取预防措施以减轻孕期空气污染相关风险的必要性。
