Acute Toxicity of Thiocyanate to Trout

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Abstract
Acutely toxic effects of thiocyanate (SCN−) were studied in brook trout Salvelinus fontinalis and rainbow trout Salmo gairdneri exposed to concentrations of up to 518 mg/L SCN−. These fishes were capable of accumulating thiocyanate against its concentration gradient and at relatively rapid rates dependent upon the exposure SCN− concentration, fish size, and anionic composition of the exposure water. Uptake of thiocyanate was inhibited by external chloride, was accompanied by a decline in the plasma Cl− concentration, and, therefore, presumably involved substitution of SCN− for Cl− at the HCO 3−/Cl− exchange sites of the gill. Endogenous conversion of thiocyanate to cyanide was detected in exposed trout; the molar equilibrium ratio of SCN− to HCN in blood was approximately 664:1. Determinations of 96‐h median lethal concentrations were of limited value in assessing the toxicity of thiocyanate because of anomalous deaths of exposed fish. These deaths were characterized by convulsions, gasping, loss of equilibrium and buoyancy, flaring of the operculae, darkening of the skin epithelium and, within minutes, cessation of ventilation and extreme rigor. This sudden death syndrome (SDS) could be triggered by strenuous exercise, abrupt changes in photoperiod, and increased levels of spontaneous activity. The SDS may involve a direct effect of SCN− on neuromuscular functioning. Prevalence of SDS was closely correlated with the plasma thiocyanate concentration; SDS occurred in half the fish when plasma concentrations reached approximately 250 mg/L SCN−.

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