ASCITES, PREMATURE EMERGENCE, INCREASED GONADAL CELL APOPTOSIS, AND CYTOCHROME P4501A INDUCTION IN PINK SALMON LARVAE CONTINUOUSLY EXPOSED TO OIL-CONTAMINATED GRAVEL DURING DEVELOPMENT

Development of pink salmon (Oncorhynchus gorbuscha) incubating in grav el contaminated with weathered Prudhoe Bay crude oil was retarded at c oncentrations as low as 55.2 mu g oil/g gravel. Larvae exposed to vari ous levels of oil contamination were sampled 4 weeks before emergence, at emergence, and 13 days after emergence for histopathology (quantit ative and semiquantitative) and cytochrome P4501A (CYP1A) induction (u sing immunohistochemical staining). A subset of postemergent fish was not fed. Hydrocarbon analysis by gas chromatography and mass spectrosc opy revealed that tissue uptake of polynuclear aromatic hydrocarbons ( PAH) was mediated by oil's dissolution in water, with significant biol ogical effects when the peak total PAH concentration in water was as l ow as 4.4 mu g/L. Oil-related effects included induction of CYP1A, dev elopment of ascites, and increased mortality. Several oil-related chan ges were indicative of premature emergence. Compared with control fish , for example, exposed fish of the same age and emerging on the same d ay had greater amounts of yolk and hepatocellular glycogen, increased apoptosis of gonadal cells and midventral skin cells, and less food in the gastrointestinal tract. Histological features were similar within groups of larvae sampled 4 weeks before and 13 days after emergence, and oil-induced changes were not affected by feeding during the first 13 days after emergence. Increased gonadal cell apoptosis may be relat ed to later reproductive impairment documented in field studies of pin k salmon up to 4 years after the Exxon Valdez oil spill.