CYP1A Induction and Blue Sac Disease in Early Life Stages of White Suckers (Catostomus commersoni) Exposed to Oil Sands

Abstract

The objectives of this study were to evaluate the influence of natural oil sands on the early developmental stages of white sucker (Catostomus commersoni) and to determine whether biochemical responses in this species were similar to native fish caught in the Athabasca Oil Sands area. Early life stage (ELS) sediment toxicity tests were conducted using controls, reference sediments, natural oil sands, and industrially contaminated (wastewater pond) sediments collected from sites along the Athabasca River, Alberta (Canada). Eggs and larvae were observed for mortality, hatching, deformities, growth, and cytochrome P-4501A (CYP1A) activity using immunohistochemistry. E-Nat-, S-Nat-, and wastewater pond sediment-exposed groups showed significant premature hatching, reduced growth, and exposure-dependent increases in ELS mortality and larval malformations relative to controls. The most common larval deformities included edemas (pericardial, yolk sac, and subepidermal), hemorrhages, and spinal defects. Juveniles exposed to oil sands and wastewater pond sediments (96 h) demonstrated significantly increased 7-ethoxyresorufin–O-deethylase (EROD) activity (30- to 50-fold) as compared to controls. Reference sediment-exposed groups and water controls demonstrated reliable embryo and larval survival, minimal malformations, and negligible CYP1A staining. These observed signs of blue sac disease (ELS mortality, malformations, growth reductions, CYP1A activity induction) may produce deleterious reproductive effects in natural fish populations exposed to oil sands mixtures.This research was funded by grants from the Toxic Substances Research Initiative (Project 187) through Health Canada, Panel on Energy Research and Development, and the Natural Sciences and Engineering Council of Canada (PVH). M. Colavecchia was supported by scholarships awarded by OGS, Canadian Network of Toxicology Centres, and Petro-Canada. The authors thank the following individuals for their technical assistance with the field sampling program: R. Neurtherander (NWRI), B. Crosley, M.Conly (CWS), Golder Associates (K. Allen and M. Ezekiel), Regional Aquatics Monitoring Program, Suncor Energy (A. Cummins), Syncrude Canada (T. VanMeer, N. Rutley), M. Bowerman, and A. Winchester (Queen's University). We thank G. Fodor (DFO), Dr. P. Akhtar (Queen's University), B. Blunt, M. Baker (NWRI), S. Cagampan, and S. Backus (NLET) for their enthusiastic laboratory assistance. Portions of this research were presented at the 2003 Annual Aquatic Toxicity Workshop (Thirtieth Annual Meeting s, p. 90). Useful comments by Dr. S. Kacew and two anonymous reviewers helped improve an earlier draft of this article.