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Effects of PM2.5 and gases exposure during prenatal and early-life on autism-like phenotypes in male rat offspring.
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2020-01-29 , DOI: 10.1186/s12989-020-0336-y
Baharan Emam 1 , Abbas Shahsavani 1, 2 , Fariba Khodagholi 3 , Saeed Motesaddi Zarandi 1 , Philip K Hopke 4, 5 , Mostafa Hadei 6, 7 , Hamidreza Behbahani 3 , Maryam Yarahmadi 8
Affiliation  

Epidemiological studies have reported associations between elevated air pollution and autism spectrum disorders (ASD). However, we hypothesized that exposure to air pollution that mimics real world scenarios, is a potential contributor to ASD. The exact etiology and molecular mechanisms underlying ASD are not well understood. Thus, we assessed whether changes in OXTR levels may be part of the mechanism linking PM2.5/gaseous pollutant exposure and ASD. The current in-vivo study investigated the effect of exposure to fine particulate matter (PM2.5) and gaseous pollutants on ASD using behavioral and molecular experiments. Four exposure groups of Wistar rats were included in this study: 1) particulate matter and gaseous pollutants exposed (PGE), 2) gaseous pollutants only exposed (GE), 3) autism-like model (ALM) with VPA induction, and 4) clean air exposed (CAE) as the control. Pregnant dams and male pups were exposed to air pollutants from embryonic day (E0) to postnatal day (PND21). The average ± SD concentrations of air pollutants were: PM2.5: 43.8 ± 21.1 μg/m3, CO: 13.5 ± 2.5 ppm, NO2: 0.341 ± 0.100 ppm, SO2: 0.275 ± 0.07 ppm, and O3: 0.135 ± 0.01 ppm. The OXTR protein level, catalase activity (CAT), and GSH concentrations in the ALM, PGE, and GE rats were lower than those in control group (CAE). However, the decrements in the GE rats were smaller than other groups. Also in behavioral assessments, the ALM, PGE, and GE rats demonstrated a repetitive /restricted behavior and poor social interaction, but the GE rats had weaker responses compared to other groups of rats. The PGE and GE rats showed similar trends in these tests compared to the VPA rats. This study suggested that exposure to ambient air pollution contributed to ASD and that OXTR protein may serve as part of the mechanism linking them.

中文翻译:

产前和生命早期PM2.5和气体暴露对雄性大鼠后代自闭症样表型的影响。

流行病学研究报告了空气污染加剧与自闭症谱系障碍(ASD)之间的关联。但是,我们假设模拟现实情况的空气污染可能是导致自闭症的原因之一。尚不清楚ASD的确切病因和分子机制。因此,我们评估了OXTR水平的变化是否可能是PM2.5 /气态污染物暴露与ASD关联的机制的一部分。当前的体内研究使用行为和分子实验研究了暴露于细颗粒物(PM2.5)和气态污染物对ASD的影响。Wistar大鼠分为四个暴露组:1)暴露的颗粒物和气态污染物(PGE),2)仅暴露的气态污染物(GE),3)具有VPA诱导的自闭症模型(ALM),和4)暴露在清洁空气中(CAE)作为对照。从胚胎天(E0)到产后一天(PND21),怀孕的水坝和雄性幼崽都暴露于空气污染物中。空气污染物的平均±SD浓度为:PM2.5:43.8±21.1μg/ m3,CO:13.5±2.5 ppm,NO2:0.341±0.100 ppm,SO2:0.275±0.07 ppm,O3:0.135±0.01 ppm。ALM,PGE和GE大鼠的OXTR蛋白水平,过氧化氢酶活性(CAT)和GSH浓度均低于对照组(CAE)。然而,GE大鼠的减量小于其他组。同样在行为评估中,ALM,PGE和GE大鼠表现出重复/受限行为和不良的社交互动,但与其他组大鼠相比,GE大鼠的反应较弱。与VPA大鼠相比,PGE和GE大鼠在这些测试中显示出相似的趋势。
更新日期:2020-01-29
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