The Relationships among CYP1A Induction, Toxicity, and Eye Pathology in Early Life Stages of Fish Exposed to Oil Sands

Abstract

Exposure of the early life stages of fish to oil sands constituents is associated with mortality and larval malformations such as edemas, hemorrhages, and skeletal, craniofacial, and eye defects. In fathead minnow (Pimephales promelas) and white sucker (Catostomus commersoni) larvae, indices of total eye pathology increased significantly following oil sands exposure. Structural, cytoplasmic, inflammatory, and degenerative eye alterations included poor retinal differentiation, microphthalmia, optic fissures, dysphasic retinas and lenses, inflammatory infiltrates, retinal epithelial lifting, and necrotic foci. Cytochrome P-4501A (CYP1A) was expressed in ocular (retina, lens) and kidney endothelial tissues, as indicated by immunohistochemistry. Although the kinetics of exposure-response curves for mortality and CYP1A expression were similar in both species, species differences in the magnitude and sensitivity of the responses were observed. Oil sands were twofold more toxic to fathead minnows (TPAH LC50 = 47–330 μg/g) than to white sucker (TPAH LC50  = 95–860 μg/g) larvae. For both species, larval mortality was significantly related to CYP1A protein concentrations in kidneys, and severity of these effects rose with oil sands exposure. The relationships among eye damage, mortality, and CYP1A indices warrants further investigation, and may lead to the use of CYP1A induction as an indicator of adverse effects rather than just contaminant exposure.

This research was supported by the Toxic Substances Research Initiative of Health Canada and Environment Canada, Panel on Energy Research and Development, and the Natural Sciences and Engineering Council of Canada (PVH). Further support was provided by Ontario Graduate Scholarships, Canadian Network of Toxicology Centres, and Petro-Canada (MVC). We gratefully acknowledge C. Khan, M. Bauder, L. Svatek, and C. Sullivan for their assistance with histology and microscopy. We thank B. Blunt, S. Backus, S. Cagampan, G. Williston, and G. Tetreault for their laboratory assistance. Special thanks to Suncor Energy (A. Cummins) and Syncrude Canada, Ltd. (T. Van Meer and N. Rutley) for their field support and guidance on site. Portions of this research were presented at the 2005 Annual Aquatic Toxicity Workshop (Thirty-Second Annual Meeting Abstracts, p. 82).