Abstract：
To highlight the key role of global warming on the toxicity of contaminants, the cardiovascular toxicity of nanoparticles (NPs) was estimated in developing zebrafish (Danio rerio) at different exposure temperatures, and the toxicity mechanisms were explored via multi-omic analyses. Polystyrene NPs (50 nm) at 0.1 mg·L-1 entered zebrafish embryos at 24 h post-fertilization and caused cardiovascular toxicity in the developing zebrafish at 27 ℃. This was explained by the down-regulation of the branched-chain amino acid and insulin signaling pathways owing to induced oxidative stress. Elevated exposure temperatures promoted the accumulation of NPs in developing zebrafish, increased the levels of oxidative stress and enhanced the oxidative phosphorylation rate in mitochondria, thus resulting in an additive effect on the mortality of zebrafish larvae. Notably, elevated exposure temperatures reduced the cardiovascular toxicity of NPs, as the effective concentration of NPs for inhibiting embryonic heartbeat rate increased from 0.1 mg·L-1 at 27 ℃ to 1.0 mg·L-1 at 30 ℃. Experiments of transgenic zebrafish Tg(myl7:GFP) and multi-omic analyses revealed that elevated temperatures enhanced the myocardial contractility of larvae, thus reducing the cardiovascular toxicity of NPs. However, the health risks of enhanced myocardial contraction caused by NP exposure at elevated temperatures requires further consideration.
摘要：
为了强调全球变暖对污染物毒性的关键作用，在不同的暴露温度下，在发展斑马鱼（Daniorerio）中估计纳米粒子（NPs）的心血管毒性，并通过多维分析探讨了毒性机制。0.1mg·L-1的聚苯乙烯NPs（50nm）在受精后24h进入斑马鱼胚胎，并在27℃下对发育中的斑马鱼造成心血管毒性。这可以通过诱导的氧化应激引起的支链氨基酸和胰岛素信号通路的下调来解释。升高的暴露温度促进了发育中的斑马鱼中NP的积累，增加氧化应激水平，增强线粒体的氧化磷酸化率，从而对斑马鱼幼虫的死亡率产生累加效应。值得注意的是,升高的暴露温度降低了NPs的心血管毒性，随着抑制胚胎心率的有效NPs浓度从27℃时的0.1mg·L-1增加到30℃时的1.0mg·L-1。转基因斑马鱼Tg（myl7：GFP）的实验和多组分析显示，升高的温度增强了幼虫的心肌收缩力，从而减少NPs的心血管毒性。然而,在升高的温度下,NP暴露导致心肌收缩增强的健康风险需要进一步考虑.
