| THE DEVELOPING FISH HEART AND LETHAL IMPACTS OF CRUDE OIL EXPOSURE |
| INCARDONA, J.P., National Oceanic and Atmospheric Administration, Northwest Fisheries Science Center, Seattle, WA, USA 98112, john.incardona@noaa.gov.
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| Exposure to crude oil during embryonic development results in a complex syndrome of abnormalities that appears common to all teleosts. To gain insight into the mechanisms underlying this syndrome and develop tools for assessing the impacts of oil spills on spawning populations of fish, we have employed the zebrafish model over the last decade in a series of studies on crude oils from various sources, as well as individual suspect chemical constituents. We found that (1) the developing heart is a primary target of crude oil impacts, (2) polycyclic aromatic compounds (PACs) in crude oil are cardiotoxic, and (3) there are at least two distinct pathways by which PAC cardiotoxicity damages the developing fish heart. Because the heart becomes functional and drives embryonic circulation while still in very early stages of morphogenesis, functional impacts secondarily affect heart form. At higher levels of toxicity, this leads to serious heart malformation, heart failure, and larval mortality. At the same time, prior mark and recapture in salmonids demonstrated that larvae that survive low-level toxicity and appear externally normal suffer mortality that is delayed into the second year of life. More recent studies by our group to be described here have both extended the mechanistic work explaining the larval-lethal impacts of crude oil exposure to non-model species (including demersal, pelagic cold, temperate and tropical species), and demonstrated that delayed mortality represents a more subtle, lesser extreme spectrum of the same processes that drive larval lethality. These mechanistic pathways suggest novel candidates for molecular indicators of fish injury following oil spills. |
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