The lampricide 3-trifluoromethyl-4-nitrophenol (TFM) interferes with intermediary metabolism and glucose homeostasis, but not with ion balance, in larval sea lamprey (Petromyzon marinus)

Although treatment of streams with the lampricide 3-trifluoromethyl-4-nitrophenol (TFM) has been highly effective for sea lamprey (Petromyzon marinus) population control in the Great Lakes, little is known about its mechanism(s) of toxicity. We investigated two hypotheses of TFM toxicity in larval sea lamprey exposed to TFM for 12 h. The first was that TFM interferes with oxidative ATP production by mitochondria, causing depletion of fuel stores in the body. The second was that TFM interferes with gill-mediated ion exchange, which eventually causes circulatory collapse. While exposure of larvae to TFM (2 mg center dot L-1) did not disturb tissue ATP stores, it led to a sustained 60% reduction in phosphocreatine (PCr) after 6 h. This was accompanied by 6- to 10-fold increases in plasma and tissue lactate, which persisted through 12 h. By 12 h, plasma glucose was nearly depleted in the five surviving lamprey, but TFM caused no appreciable changes in plasma Cl-, haematocrit, haemoglobin, or ammonia concentration. We conclude that TFM-mediated gill damage and ionic failure are not underlying mechanisms of TFM toxicity. Rather, TFM likely interferes with oxidative ATP production, leading to reduced tissue PCr stores and eventually profound hypoglycaemia that starves the nervous system of glucose, causing death.