Cardiotoxic effects of polycyclic aromatic hydrocarbons and abiotic stressors in early life stage estuarine teleosts

Following the 2010 Deepwater Horizon oil spill, extensive research has been conducted on the toxicity of oil and polycyclic aromatic hydrocarbons (PAHs) in the aquatic environment. The location and timing of the Deepwater Horizon surface slick coincided with the spawning seasons of many important pelagic and estuarine fish species. As such, there has been particular emphasis placed on the effects of PAHs on sensitive life history stages in fish, such as the embryonic and larval periods. Additionally, the spill occurred throughout the spring and summer months which, in estuaries, are marked by regular fluctuations in abiotic environmental factors such as dissolved oxygen, salinity, and temperature. Until recently, there has been little work done to elucidate the combined effects that PAHs from oil spills and adverse environmental conditions (hypoxia, increased salinity, and elevated temperatures).

Work presented in this dissertation uses next generation sequencing technology (RNA Seq) to determine differential gene expression in larval estuarine teleosts following exposure to adverse environmental conditions and PAHs. Downstream canonical pathway and toxicological function analysis were then applied to the identified differentially expressed genes (DEGs) to predict cardiotoxic responses at the organismal level. To verify the predicted responses, a phenotypic anchoring study was conducted and identified a cardiotoxic phenotype (pericardial edema) and reduced cardiac output in embryos exposed to oil. Finally, the mechano-genetic interplay governing the morphological development of the teleost heart was investigated and correlations between developmental gene expression and blood flow forces within the cardiovascular system were identified.