Niclosamide Effects on Rainbow Trout

Niclosamide (2′,5-dichloro-4′-nitrosalicylanalide) is a piscicide used to control invasive sea lamprey (Petromyzon marinus) in the Laurentian Great Lakes. It is also a molluscide used in tropical and sub-tropical freshwaters to control snail populations that are intermediate hosts to the blood flukes that causes schistosomiasis in humans. While the mechanism of niclosamide toxicity is known, its corresponding physiological effects on non-target fishes are not well-established. To better understand how niclosamide could adversely affect non-target fishes, rainbow trout (Oncorhynchus mykiss) were exposed to an environmentally relevant niclosamide concentration of 0.150 mg L􀀀 1 (measured = 0.12–0.18 mg L􀀀 1) over 9 h, during which tissues were collected for measurement of energy stores and metabolites. Niclosamide exposure reduced brain ATP and glycogen by ~50 %, and liver glycogen by ~40 %. Reductions of ATP, phosphocreatine and glycogen were also observed in muscle, with corresponding increases in pyruvate and lactate, plus development of a metabolic acidosis (~0.2 unit decrease in intracellular pH). These disturbances were consistent with impaired mitochondrial oxidative phosphorylation and greater reliance on anaerobic glycolysis to generate ATP. Notably, physiological homeostasis was restored in the brain, liver, and muscle within 24 h after depuration in fresh, niclosamide-free water. We conclude that nontarget fishes are susceptible to niclosamide, but at least in rainbow trout, the effects are readily reversed after exposure ceases. Similar approaches could be used to determine the susceptibility and resilience of other fishes to niclosamide in environments where it is required as a either a lampricide or a molluscicide.