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High-content screening in zebrafish identifies perfluorooctanesulfonamide as a potent developmental toxicant.
Environmental Pollution ( IF 7.6 ) Pub Date : 2019-10-31 , DOI: 10.1016/j.envpol.2019.113550 Subham Dasgupta 1 , Aalekhya Reddam 2 , Zekun Liu 3 , Jinyong Liu 3 , David C Volz 1
Environmental Pollution ( IF 7.6 ) Pub Date : 2019-10-31 , DOI: 10.1016/j.envpol.2019.113550 Subham Dasgupta 1 , Aalekhya Reddam 2 , Zekun Liu 3 , Jinyong Liu 3 , David C Volz 1
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Per- and polyfluoroalkyl substances (PFASs) have been used for decades within industrial processes and consumer products, resulting in frequent detection within the environment. Using zebrafish embryos, we screened 38 PFASs for developmental toxicity and revealed that perfluorooctanesulfonamide (PFOSA) was the most potent developmental toxicant, resulting in elevated mortality and developmental abnormalities following exposure from 6 to 24 h post fertilization (hpf) and 6 to 72 hpf. PFOSA resulted in a concentration-dependent increase in mortality and abnormalities, with surviving embryos exhibiting a >12-h delay in development at 24 hpf. Exposures initiated at 0.75 hpf also resulted in a concentration-dependent delay in epiboly, although these effects were not driven by a specific sensitive window of development. We relied on mRNA-sequencing to identify the potential association of PFOSA-induced developmental delays with impacts on the embryonic transcriptome. Relative to stage-matched vehicle controls, these data revealed that pathways related to hepatotoxicity and lipid transport were disrupted in embryos exposed to PFOSA from 0.75 to 14 hpf and 0.75 to 24 hpf. Therefore, we measured liver area as well as neutral lipids in 128-hpf embryos exposed to vehicle (0.1% DMSO) or PFOSA from 0.75 to 24 hpf and clean water from 24 to 128 hpf, and showed that PFOSA exposure from 0.75 to 24 hpf resulted in a decrease in liver area and increase in yolk sac neutral lipids at 128 hpf. Overall, our findings show that early exposure to PFOSA adversely impacts embryogenesis, an effect that may lead to altered lipid transport and liver development.
中文翻译：
在斑马鱼中进行高含量的筛选可确定全氟辛烷磺酰胺为有效的发育毒物。
全氟烷基物质和多氟烷基物质（PFAS）在工业过程和消费产品中已使用了数十年，导致在环境中频繁进行检测。我们使用斑马鱼胚胎筛选了38种PFAS的发育毒性，并发现全氟辛烷磺酰胺（PFOSA）是最有效的发育毒性物质，在受精后6至24小时（hpf）和6至72 hpf暴露后导致死亡率和发育异常增加。PFOSA导致死亡率和异常率的浓度依赖性增加，存活的胚胎在24 hpf时发育延迟> 12 h。0.75 hpf时开始的暴露也导致外延性浓度依赖性延迟，尽管这些影响不是由特定的敏感发育窗口驱动的。我们依靠mRNA测序来确定PFOSA诱导的发育延迟与对胚胎转录组的影响的潜在关联。相对于阶段匹配的媒介物对照，这些数据表明，暴露于PFOSA的胚胎在0.75至14 hpf和0.75至24 hpf的胚胎中，与肝毒性和脂质转运相关的途径被破坏。因此，我们测量了暴露于媒介物（0.1％DMSO）或PFOSA的0.75至24 hpf的128-hpf胚胎和暴露于24至128 hpf的纯净水的128-hpf胚胎的肝脏面积以及中性脂质，结果表明PFSEA暴露于0.75至24 hpf的胚胎导致在128 hpf时肝脏面积减少，卵黄囊中性脂质增加。总体而言，我们的研究结果表明，尽早接触PFOSA会对胚胎发生产生不利影响，这种作用可能导致脂质转运和肝脏发育改变。
更新日期：2019-11-01
中文翻译：
在斑马鱼中进行高含量的筛选可确定全氟辛烷磺酰胺为有效的发育毒物。
全氟烷基物质和多氟烷基物质（PFAS）在工业过程和消费产品中已使用了数十年，导致在环境中频繁进行检测。我们使用斑马鱼胚胎筛选了38种PFAS的发育毒性，并发现全氟辛烷磺酰胺（PFOSA）是最有效的发育毒性物质，在受精后6至24小时（hpf）和6至72 hpf暴露后导致死亡率和发育异常增加。PFOSA导致死亡率和异常率的浓度依赖性增加，存活的胚胎在24 hpf时发育延迟> 12 h。0.75 hpf时开始的暴露也导致外延性浓度依赖性延迟，尽管这些影响不是由特定的敏感发育窗口驱动的。我们依靠mRNA测序来确定PFOSA诱导的发育延迟与对胚胎转录组的影响的潜在关联。相对于阶段匹配的媒介物对照，这些数据表明，暴露于PFOSA的胚胎在0.75至14 hpf和0.75至24 hpf的胚胎中，与肝毒性和脂质转运相关的途径被破坏。因此，我们测量了暴露于媒介物（0.1％DMSO）或PFOSA的0.75至24 hpf的128-hpf胚胎和暴露于24至128 hpf的纯净水的128-hpf胚胎的肝脏面积以及中性脂质，结果表明PFSEA暴露于0.75至24 hpf的胚胎导致在128 hpf时肝脏面积减少，卵黄囊中性脂质增加。总体而言，我们的研究结果表明，尽早接触PFOSA会对胚胎发生产生不利影响，这种作用可能导致脂质转运和肝脏发育改变。
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