Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)






Rainbow trout exposed to lethal (1.5 mg/L) or sublethal (0.8 mg/L) concentrations of waterborne Zn ([Zn]w) exhibited different physiological responses. The lethal response was well-defined, consisting of hypoxemia probably due to gill damage. This in turn caused tissue hypoxia as evidenced by appearance of lactate in the blood, decrease in blood pH, and concomitant changes in related blood parameters. Exposure to lower [Zn]w resulted in changes which were less severe, and varied with water pH, and between artifical and natural soft water. At neutral pH, in artifical soft water (ASW) an alkalosis developed, while at pHw 5, or, in natural soft water at pHw 7, an acidosis occurred similar to acute exposure, but of longer onset. Decrease in arterial oxygen tension (Pa₀₂), where it occurred, was much smaller than in the acute exposure suggesting that damage to branchial epithelial tissue was minimal. Limited lactate appearance in the blood suggested that some hypoxia occurred further along the respiratory chain. The alkalosis was deemed to be a sign of less severe stress arising from altered Cl⁻/HCO⁻₃ exchange.

Exposure to pHw 9 either with or without 1.5 mg/L added Zn was rapidly lethal. Blood pH was normal despite massive accumulations of blood lactate. Un-ionized ammonia concentrations may have been high enough to exert some toxic effect.

Unidirectional branchial flux rates of Na were little altered by exposure to 0.8 mg/L Zn in natural soft water, while Cl⁻ net uptake was reduced t becoming a net loss after 60 h. Net branchial Ca²⁺ uptake was immediately abolished by 0.8 mg/L Zn and showed no subsequent recovery. Reduction in acid excretion at both gill and kidney may have been the cause of the acidosis. Measurements of whole blood and plasma Zn indicated preferential accumulation in the plasma. Possible effects of zinc on carbonic anhydrase and branchial ion exchanges are discussed.

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