Ion Flux Rates, Acid–Base Status, and Blood Gases in Rainbow Trout,Salmo gairdneri, Exposed to Toxic Zinc in Natural Soft Water

Abstract

Exposure to 0.8 mg Zn2+/L in natural soft water for up to 72 h was toxic to rainbow trout, Salmo gairdneri, causing an acid–base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78 to 7.58. Both [Formula: see text] and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high [Formula: see text] Net branchial uptake of Na+and Cl−became a net loss immediately following exposure to Zn2+, and this continued during 60 h of exposure. Net K+loss was exacerbated, and net Ca2+uptake was abolished. Unidirectional flux measurements with22Na+and36Cl−indicated an increased efflux immediately following zinc exposure. Both influx and efflux of Na+and Cl−were stimulated after 48–60 h in Zn2+. Both net branchial ammonia excretion and net branchial uptake of acidic equivalents from the water (=base loss) were greatly stimulated, the latter contributing to metabolic acidosis. Kidney function, as measured by urine flow rate and excretion of ammonia, acidic equivalents, Na+, Cl−, K+, and Zn2+, was relatively insensitive to the effects of zinc. The only renal component to be affected was Ca2+excretion, which decreased during a single flux period, possibly in response to the reduced entry of Ca2+at the gill. We conclude that toxic concentrations of zinc are capable of altering gill function so as to cause ionoregulatory and acid–base disturbances without disturbance of [Formula: see text].