University of Alaska-Fairbanks Fisheries Division, University of Alaska-Fairbanks Juneau Center, Juneau, AK 99801, USA.
Proc Natl Acad Sci U S A. 2011 Apr 26;108(17):7086-90. doi: 10.1073/pnas.1019031108. Epub 2011 Apr 11.
Exposure to high concentrations of crude oil produces a lethal syndrome of heart failure in fish embryos. Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubiquitous components of petroleum. Here, we show that transient embryonic exposure to very low concentrations of oil causes toxicity that is sublethal, delayed, and not counteracted by the protective effects of cytochrome P450 induction. Nearly a year after embryonic oil exposure, adult zebrafish showed subtle changes in heart shape and a significant reduction in swimming performance, indicative of reduced cardiac output. These delayed physiological impacts on cardiovascular performance at later life stages provide a potential mechanism linking reduced individual survival to population-level ecosystem responses of fish species to chronic, low-level oil pollution.
暴露在高浓度的原油中会导致鱼类胚胎出现致命的心力衰竭综合征。这种死亡率是由多环芳烃（PAHs）引起的，多环芳烃是石油的普遍成分，具有心脏毒性。在这里，我们表明，胚胎在非常低浓度的油中短暂暴露会导致毒性，这种毒性是亚致死性的、延迟的，而且不会被细胞色素 P450 诱导的保护作用所抵消。在胚胎期暴露于油后近一年，成年斑马鱼的心脏形状出现细微变化，游泳能力显著下降，表明心输出量减少。这些对心血管性能的延迟生理影响在以后的生命阶段提供了一个潜在的机制，将个体存活率的降低与鱼类物种对慢性、低水平石油污染的种群水平生态系统反应联系起来。
