Abstract

Hydrocyanic acid, a common industrial pollutant, caused severe damage to developing embryos of Atlantic salmon (Salmo salar) when newly fertilized eggs were continually exposed to sublethal concentrations of the poison (0.01–0.10 mg/L HCN) up to the end of the sac-fry stage. Each test group was held in small flow-through basins with the toxicant metered through the entire experimental period. At 0.08 and 0.10 mg/L, cyanide delayed hatching by 6–9 days but all concentrations reduced hatching success by about 15–40%. During incubation conversion of yolk into body tissues was reduced at all concentrations above 0.01 mg/L. The most striking effect of cyanide, however, was a high incidence of abnormalities ranging from about 6% at 0.01 mg/L to about 19% at 0.10 mg/L. During incubation cyanide had reduced development, but after hatching survival was not affected and growth of cyanide-exposed sac fry was either equal to or faster than that of the controls as a result of higher yolk conversion efficiency. The total metabolism of the sac fry was estimated to explain this phenomenon. To protect salmon streams during embryo–larval stages, the maximum acceptable toxicant concentration for cyanide should not exceed 0.005 mg/L HCN. Key words: cyanide pollution, eggs and fry, embryogenesis, teratogenic effects, Atlantic salmon

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