Key result
Embryonic crude oil exposure alters adult zebrafish heart morphology and impairs long-term swimming performance.
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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.
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Hicken et al. (2011) studied Cardiotoxicity from embryonic crude oil exposure. Transient embryonic exposure to very low concentrations of crude oil was evaluated on Cardiac morphology (heart shape) and aerobic capacity (swimming performance). Transient embryonic exposure to low-level crude oil altered adult heart shape and significantly reduced swimming performance nearly 1 year later in zebrafish.
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