Ascites, premature emergence, increased gonadal cell apoptosis, and cytochrome P4501A induction in pink salmon larvae continuously exposed to oil-contaminated gravel during development

Abstract

Development of pink salmon (Oncorhynchus gorbuscha) incubating in gravel contaminated with weathered Prudhoe Bay crude oil was retarded at concentrations as low as 55.2 μg oil/g gravel. Larvae exposed to various levels of oil contamination were sampled 4 weeks before emergence, at emergence, and 13 days after emergence for histopathology (quantitative and semiquantitative) and cytochrome P4501A (CYP1A) induction (using immunohistochemical staining). A subset of postemergent fish was not fed. Hydrocarbon analysis by gas chromatography and mass spectroscopy revealed that tissue uptake of polynuclear aromatic hydrocarbons (PAH) was mediated by oil's dissolution in water, with significant biological effects when the peak total PAH concentration in water was as low as 4.4 μg/L. Oil-related effects included induction of CYP1A, development of ascites, and increased mortality. Several oil-related changes were indicative of premature emergence. Compared with control fish, for example, exposed fish of the same age and emerging on the same day 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 related to later reproductive impairment documented in field studies of pink salmon up to 4 years after the Exxon Valdez oil spill.