Document Type

Thesis

Degree Name

Master of Science (MSc)

Department

Biology

Program Name/Specialization

Integrative Biology

Faculty/School

Faculty of Science

First Advisor

Jim McGeer

Advisor Role

Thesis Supervisor

Abstract

During chronic exposure to Cd or other metals, freshwater fish generally undergo physiological changes that results in acclimation, following a phase of damage and subsequent repair. The mechanisms associated with deleterious cellular effects induced by Cd throughout long-term exposures are less understood than those of acute toxicity, and may relate to an over-production of reactive oxygen species. The objectives of the present study were to examine the changes in, and relationship between, tissue-specific oxidative damage and antioxidant response, as well as plasma ionic regulation and tissue accumulation, in two freshwater salmonids throughout chronic Cd exposure. Rainbow trout (O. mykiss) or lake whitefish (C. clupeaformis) were exposed to either 0 (control), 0.8 or 2.0 μg Cd/L in moderately hard water (140 mg CaCO3/L) for one month, and gills, liver, kidney and plasma were sampled throughout exposure. Measured responses included plasma Ca2+ and Na+, as well as total tissue Cd burden and indicators of oxidative stress (lipid peroxidation, protein damage and enzymatic antioxidant defense (as catalase activity)) in tissues. Fish of either species experienced initial disruptions in plasma ion levels and/or mortality, which were associated with elevated Cd burdens in the gills. Exposure to sublethal Cd was sufficient to cause early oxidative lipid and/or protein damage in the liver and kidney, and subsequent recovery may relate to the elevated and sustained CAT response in these tissues, in addition to other cellular defenses. Long-term lipid peroxidation was found only in the gills of exposed rainbow trout, suggesting that the antioxidant capacities and/or detoxification mechanisms of the gills may be different than those in other tissues or of lake whitefish. Overall, this study demonstrates that the degree and pattern of oxidative damage and enzymatic antioxidant defense induced by Cd during chronic waterborne exposure varies amongst tissues and species.

Convocation Year

2011

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