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1 1 1 1 1 1 1 28 BIOLOGICAL REPORT 65(1.23) gelding free c}•anide on direct exposure to sun- light-and the nickelocyanide ion complex are not likely to be of practical importance (Doudorofi 1976). Toxicity to aquatic organisms of organic cyanide compounds, such as lactonitrile, is similar to that of inorganic cyanides because they usually undergo rapid hydrolysis in water to free cyanide (Towill et al. 1978). There is general agreement that total cyanide concentrations in water in most cases will overestimate the actual cyanide toxicity to aquatic organisms, and that the analytically de- termined HCN concentration in cyanide-polluted waters is considered to be the most reliable index of toxicity (DoudorofT 1976; Smith et al. 1979; EPA 1980; Abe] and Garner 1986). Cyanide acts rapidly in aquatic environments, does not persist for extended periods, and is highly species selective; organisms usually recover quickly on removal to clean water. The critical sites for cyanide toxicity in freshwater organisms include the gills, egg capsules, and other sites where gaseous exchange and osmoregulatory proc- esses occur. On passing through a semipermeable membrane, the HCN molecules are usually dis- tributed by way of the circulatory system to vari- ous receptor sites where toxic action or detoxification occurs (Leduc 1984). Once in the general circulation, cyanide rapidly inhibits the electron transport chain of vita] organs. Signs of distress include increased ventilation, gulping for air at the surface, erratic swimming movements, muscular incoordination, convulsions, tremors, sinking to the bottom, and death with widel}' ex- tended gill covers (Leduc 1981, 1984). The acute mode of action of HCTQ is limited to binding those porphprins that contain Fe•', such as cvtochrome oxidase, hydroperoxidases, and methemoglobin. At lethal levels, cyanide is primarily a respiratory po»on and one of the most rapidly effective toxi- cants known (Leduc et al. 1982). The detoxi- fication mechanism of cyanide is mediated b}~ thiosulfate sulfur transferase, also known as rhodanese. This enzyme is widely distributed in animals, including fish liver, gills, and kidney. Rhodanese plays a kep role in sulfur metabolism, and catalyzes the transfer of a sulfane-sulfur group to a thiophilic group (Leduc 1984). Thio- sulfateadministered in the water with cyanide re- ducedthe toxicit}• ofcyanide tofish, presumably by increasing the detoxification rate of cyanide to thiocvanate (Toa•i]] et al. 1978). Additive ormore-than-additive toxicity offree cyanide to aquatic fauna has been reported in com- bination with ammonia (Smith et al. 1979; Leduc et a1.1982;Alabasteret a1.1983;Leduc1989)orar- senic (Leduc 1984). However, conflicting reports on the toxicity of mixtures of HCN with zinc or chromium (Towill et al. 1976; Smith et al. 1979; Leduc et a1. 1982; Leduc 19841 require clarifica- tion. Formation of the nickelocyanide complex markedly reduces the toxicity of both cyanide and nickel at high concentrations in alkpline pH. At lower concentrations and acidic pH, solutions in- crease in toxicity by more than 1,000 times, owing to dissociation of the metallocyanid@ complex to form hydrogen cyanide (Towill et al. 1978). Mix- tures of cyanide and ammonia may interfere with seaward migration of Atlantic salmoh smolts un- der conditions of low dissolved oxygen (Alabaster et al. 1983 ). The 96-h toxi ci ty of m ixtutes of sodi um cyanide and nickel sulfate to fathead minnows is influenced by water alkalinity and pH. Toxicity de- creased with increasing alkalinity and pH from 0.92 mg CN/L at 5 mg CaCOa/L. and pH 6.5; to 1.4 mg CNlL at 70 mg CaCO.,JL and pH 7,5; to 730 mg CN/L at 192 mg CaCO:/L and pH S.U (DoudorofC 1956). Numerous biological and abioti¢ factors are known to modify the biocidal propertigs offree cya- nide,includingwater pH,temperature. and oxygen content; life stage, condition, and spe#ies assayed; previous exposure W cyanide compounds; presence of otherchemicals; and initial dose te5led. There is general agreement that cyanide is more toxic to freshwater fish under conditions of ]Ow dissolved oxygen (Doudorofl' 1976; Towill et al. 1978; Smith et al. 1979; EPA 1980; Leduc 1984); that pH levels within the range 6.8-8.3 had little effect on cya- nide toxicity but enhanced toxicity 8t acidic pH (Smith et al. 1979; EPA 1980; Leduc et al. 1982; Leduc 1984); that juveniles and adu9ts were the most sensitive life stages tested and embryos and sac fr}• the mast resistant (Smith et al. 1978, 1979; EPA 1980; Leduc 1984); and that substantial in- terspecies variability exists in sensitivit}• to free cyanide (Smith et al. 1979; EPA 1980). Initial dose and water temperature both modify the biocidal properties of HCN to freshwater tel eosts. At slowly lethal concentrations (i.e., <10 ug HCN/L), cyanide was more toxic at lower temperatures; a t high, rap- idlylethal HCN concentrations, cyanide was more toxic at elevated temperatures (liovaos and Leduc 1982a, 1982b; Leduc et al. 1982; Leduc 1984). By contrast, aquatic invertebrates were most sensi- tive to HCI~T at elevated water temperatures, re- gardless of dose (Smith et al. 1979). Season and exercise modiC}• the lethality of HCN to juvenile