Developmental exposures to perfluorooctanesulfonic acid (PFOS) impact embryonic nutrition, pancreatic morphology, and adiposity in the zebrafish, Danio rerio.

Developmental exposures to perfluorooctanesulfonic acid (PFOS) impact embryonic nutrition, pancreatic morphology, and adiposity in the zebrafish, Danio rerio.
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全氟辛烷磺酸(PFOS)的发育暴露影响斑马鱼(Danio rerio)的胚胎营养、胰腺形态和肥胖。

DOI:
10.1016/j.envpol.2021.116644
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发表时间:
2021-04-15
期刊:
Environmental pollution (Barking, Essex : 1987)
影响因子:
--
通讯作者:
Timme-Laragy AR
Timme-Laragy AR
中科院分区:
其他
文献类型:
--
作者:
Sant KE;Annunziato K;Conlin S;Teicher G;Chen P;Venezia O;Downes GB;Park Y;Timme-Laragy AR

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全氟辛烷磺酸(PFOS)是一种持久性环境污染物,以前在消费品表面活性剂和工业灭火泡沫中发现过。全氟辛烷磺酸与整个生命周期的代谢功能障碍,包括糖尿病和肥胖症有着广泛的联系。然而,胚胎环境对代谢性疾病的贡献仍然没有得到表征。本研究旨在确定全氟辛烷磺酸对胚胎代谢、胰腺发育和肥胖症的干扰,这些干扰是由于发育期和亚慢性接触全氟辛烷磺酸造成的,并持续到后期幼虫和幼年期。斑马鱼胚胎在发育期(受精后1-5天; dpf)或亚慢性期(1- 1-5 dpf)暴露于16或32 μM的全氟辛烷磺酸。胚胎脂肪酸和常量营养素的浓度和过氧化物酶体增殖物激活受体(PPAR)亚型的表达进行了定量。在15和30 dpf评估胰岛形态学,并在15 dpf评估肥胖和鱼的行为。全氟辛烷磺酸在4 dpf时增加了月桂酸(C12:0)和肉豆蔻酸(C14:0)饱和脂肪酸的浓度,并降低了过氧化物酶体增殖物激活受体基因的表达。在15 dpf仔鱼和30 dpf幼鱼中,异常胰岛形态、主要胰岛面积和肥胖的发生率增加。总之,这些数据表明,胚胎期是对全氟辛烷磺酸暴露作出反应的代谢程序的一个敏感窗口期,仅这些早期暴露就可能在生命过程后期产生持续影响。
Perfluorooctanesulfonic acid (PFOS) is a persistent environmental contaminant previously found in consumer surfactants and industrial fire-fighting foams. PFOS has been widely implicated in metabolic dysfunction across the lifespan, including diabetes and obesity. However, the contributions of the embryonic environment to metabolic disease remain uncharacterized. This study seeks to identify perturbations in embryonic metabolism, pancreas development, and adiposity due to developmental and subchronic PFOS exposures and their persistence into later larval and juvenile periods. Zebrafish embryos were exposed to 16 or 32 μM PFOS developmentally (1–5 days post fertilization; dpf) or subchronically (1–15 dpf). Embryonic fatty acid and macronutrient concentrations and expression of peroxisome proliferator-activated receptor (PPAR) isoforms were quantified in embryos. Pancreatic islet morphometry was assessed at 15 and 30 dpf, and adiposity and fish behavior were assessed at 15 dpf. Concentrations of lauric (C12:0) and myristic (C14:0) saturated fatty acids were increased by PFOS at 4 dpf, and PPAR gene expression was reduced. Incidence of aberrant islet morphologies, principal islet areas, and adiposity were increased in 15 dpf larvae and 30 dpf juvenile fish. Together, these data suggest that the embryonic period is a susceptible window of metabolic programming in response to PFOS exposures, and that these early exposures alone can have persisting effects later in the lifecourse.
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