Effects of Acute and Sub-Chronic Waterborne Thallium Exposure on Ionoregulatory Enzyme Activity and Oxidative Stress in Rainbow Trout (Oncorhynchus mykiss).

The mechanisms of acute (96 h) and sub-chronic (28-d) toxicity of the waterborne trace metal thallium (Tl) to rainbow trout (Oncorhynchus mykiss) were investigated. Specifically, effects on branchial and renal ionoregulatory enzymes (sodium/potassium ATPase and proton ATPase) and hepatic oxidative stress endpoints (protein carbonylation, glutathione content and activities of catalase and glutathione peroxidase) were examined. Fish (19-55 g) were acutely exposed to 0 (control), 0.9 (regulatory limit), 2004 (half the acute median lethal concentration) or 4200 (acute median lethal concentration) µg Tl L -1 or sub-chronically exposed to 0, 0.9 or 141 (an elevated environmental concentration) µg Tl L -1 . The only effect following acute exposure was a stimulation of renal H + -ATPase activity at the highest Tl exposure concentration. Similarly, the only significant effect of sub-chronic Tl exposure was an inhibition of branchial NKA activity at 141 µg Tl L -1 , an effect that may reflect the interaction of Tl with potassium ion handling. Despite significant literature evidence for effects of Tl on oxidative stress, there were no effects of Tl on any such endpoint in rainbow trout, regardless of exposure duration or exposure concentration. Elevated basal levels of antioxidant defences may explain this finding. These data suggest that ionoregulatory perturbance is a more likely mechanism of Tl toxicity than oxidative stress in rainbow trout, but is an endpoint of relevance only at elevated environmental Tl concentrations.