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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.

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Diagnostic criteria are presented for degenerative, inflammatory, nonneoplastic proliferative, and neoplastic lesions in the liver of medaka (Oryzias latipes), a small fish species frequently used in carcinogenesis studies. The criteria are the consensus of a Pathology Working Group (PWG) convened by the National Toxicology Program. The material examined by the PWG was from medaka exposed to N-nitrosodiethylamine for 28 days, removed to clean water, and sacrificed 4, 6, or 9 mo after initiation of exposure. Degenerative lesions included hepatocellular intracytoplasmic vacuolation, hepatocellular necrosis, spongiosis hepatis, hepatic cysts, and hepatocellular hyalinization. Inflammatory lesions consisted of granulomas, chronic inflammation, macrophage aggregates, and focal lymphocytic infiltration. Nonneoplastic proliferative lesions comprised foci of cellular alteration (basophilic focus, eosinophilic focus, vacuolated focus, and clear cell focus) and bile duct hyperplasia. Neoplastic lesions included hepatocellular adenoma, hepatocellular carcinoma, cholangioma, and cholangiocarcinoma. Two lesions composed mainly of spindle cells were noted, hemangiopericytoma and spindle cell proliferation. Rather than being an exhaustive treatment of medaka liver lesions, this report draws from the published literature on carcinogen-induced liver lesions in medaka and other fish species and attempts to consolidate lesion criteria into a simplified scheme that might be useful to pathologists and other researchers using medaka lesions for risk assessment or regulatory purposes.

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