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

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Abstract
Exposure to 0.8 mg Zn2+/l in natural soft water for up to 72 h was toxic to rainbow trout, S. gairdneri, causing an acid-base disturbance and net branchial ion losses. Mean arterial pH fell from 7.78-7.58. Both PascalCO2 and lactate rose, indicating a mixed respiratory and metabolic acidosis, despite maintenance of high PascalO2. 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 with 22Na+ and 36Cl- indicated an increased efflux immediately following Zn 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 form 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 Zn. 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. Toxic concentrations of Zn are capable of altering gill function so as to cause ionoregulatory and acid-base disturbances without disturbance of PaO2.
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