Hypoxia exacerbates the cardiotoxic effect of the polycyclic aromatic hydrocarbon, phenanthrene in Danio rerio

- Co-exposure to hypoxia and phenanthrene caused up to a 99% decrease in hear rate.
- Bradycardia was accompanied by a similar decrease in cardiac output and blood flow.
- Development was also slowed with co-exposure but larvae recovered post exposure.

The Deepwater Horizon oil spill of 2010 released a mixture of polycyclic aromatic hydrocarbons (PAHs) into the Gulf of Mexico presenting a complex exposure regime for native species. Concurrently, the Gulf has experienced an increase in hypoxic events due to agricultural runoff from the Mississippi River outflow. This combination presents a unique physiological challenge to native species and a challenge for researchers. The purpose of this study was to determine how the cardiotoxic PAH, phenanthrene interacts with hypoxia to affect the cardiovascular system of larval zebrafish (Danio rerio). We exposed zebrafish larvae to 0, 1, 100, and 1000 μg/L of phenanthrene in combination with normoxia and hypoxia. At late hatching, video of hearts and vessels were used to measure heart rate (ƒH), stroke volume (SV), cardiac output (Q), red blood cell velocity, and caudal vessel diameter. We found that the highest concentration of phenanthrene caused a 58, 80, and 84% decrease in ƒH, Q, and arterial red blood cell velocity in normoxia and an 88, 98, and 99% decrease in hypoxia, respectively. Co-exposed larvae also experienced higher rates of edema and lordosis in addition to a 33% increase in mortality rate with co-exposure to hypoxia at the 1000 μg/L concentration of phenanthrene. At 12 dpf, baseline swimming behavior was similar between treatments indicating partial recovery from embryonic exposure. This study shows that phenanthrene decreases cardiac parameters, most significantly heart rate and that this effect is exacerbated by simultaneous exposure to hypoxia.