Chronic cyanide poisoning of rainbow trout and its effects on growth, respiration, and liver histopathology

Abstract

Cyanide markedly affected growth and resting metabolic rate while causing degenerative hepatic necrosis in juvenile rainbow trout (Salmo gairdneri, Richardson). This was revealed during two experiments performed in continuously renewed water at 12.5 degree C with fish fed a restricted artificial diet and exposed to assayed cyanide concentrations of 0.00, 0.01, 0.02, or 0.03 mg/L hydrogen cyanide (HCN) for 18 days. At 0.02 and 0.03 mg/L, HCN growth was reduced by 40 to 95% after 18 days. At all concentrations, cyanide caused a severe initial repression of specific growth rate, followed by a highly significant increase which was insufficient to compensate for the original repression. Previous exposure to cyanide promoted a higher resting metabolic rate during the six days following exposure, the effect increasing with cyanide concentration. At all concentrations tested, widespread cyanide-induced degenerative necrosis of hepatocytes was observed; it was more intense at higher cyanide concentrations and well established even at 0.01 mg/L HCN.

Histopathological Studies on Some Organs of Oreochromis Niloticus, Tilapia Zillii and Synodontis Schall From El-Salam Canal, Egypt

“…Histopathological changes in the liver of fish as a result of exposure to toxicants have been studied by several authors (Couch, 1975, Major et al, 1975, Li et al, 1978, Sastry and Malik, 1979, Dixon and Leduc, 1981and Desai et al, 1984. Several histopathological changes in the liver were also observed in ruffe, gymnocephalus cernua, collected from Elbe Estuary contaminated by domestic, industrial and agricultural pollutants (Heidemarie and Peters, 1985), in Atlantic tomcod, Microgadus tomcod, collected from contaminated Hudson River (Cormier, 1986), in Tilapia nilotica exposed to diazinon (Issa and Gabr, 1989), in Tilapia nilotica exposed to fluorine and sulphur emitting from factory of fertilizer (Aly et al, 1992), in Clarias lazera exposed to bayluscide (Hamzaef aL, 1996), in Tilapia zillii exposed to lindane (Mourad etal, 1999) and in Oreochromis niloticus and Tilapia zillii collected from the southern region of Lake Manzalah contaminated with domestic, industrial and agricultural pollutants (Mohamed, 2001b).…”

Trends Determined by Cyanide Testing on Marine Aquarium Fish in the Philippines

“…The cyanide ion (CN -) has an affinity for metal-centered biomolecules and will bind to various enzymes and molecules (e.g., methemoglobin) to form relatively stable, but reversible, complexes. Effects on oxygen metabolism result in the disruption of physiological functions in fish and damage to the liver, spleen, heart, and brain (Dempster and Donaldson 1974;Dixon and Leduc 1981;Leduc 1984;Hall and Bellwood 1995;Hanawa et al 1998). Even if fish survive the initial pulse-exposure to high levels of cyanide, they are subject to a high delayed mortality (>80%) during export to other countries (Rubec 1986(Rubec , 1987b(Rubec , 1987c(Rubec , 1987d(Rubec , 1988Rubec and Sundararajan 1991;Rubec et al 2001aRubec et al , 2001b.…”

Acute and Sub Lethal Effect of Potassium Cyanide on the Behaviour and ATPase Enzyme Activity in the Freshwater Fish, <i>Clarias</i> <i>gariepinus </i>(Catfish)

“…Cyanide toxicity has been attributed to the presence of HCN derived from dissociation of the complexes that penetrate cells wall (Pablo et al, 1996). Major effects of cyanide on fish had been observed to include; growth inhibition (Dixon and Leduc, 1981), behavioural alterations (Shwetha and Hosetti, 2009), hypoxia (Dube and Hosetti, 2011) and susceptibility to predation (Eisler, 1991). Shwetha et al (2012) reinstated the effects of cyanide on fish and the impact it might have on human health.…”