Contrasting physiological responses between invasive sea lamprey and non-target bluegill in response to acute lampricide exposure.

Abstract Control of invasive sea lamprey (Petromyzon marinus) in the Laurentian Great Lakes includes widespread application of lampricides which consist of two active compounds, 3-trifluoromethyl-4-nitrophenol (TFM) & niclosamide. The toxicological action of these lampricides is thought to result from inhibition of aerobic energy synthesis, with TFM having a relatively selective action against lampreys. While toxicity (i.e. lethal concentrations [LC]) has been reported for a wide range of aquatic species and the physiological effects of TFM characterized, the impacts associated with exposure to niclosamide and TFM;niclosamide mixtures are poorly characterized in non-target fishes despite being an important consideration for management and conservation. Therefore, focusing on responses associated with energy metabolism, we quantified and compared the physiological responses of larval sea lamprey and bluegill (Lepomis macrochirus), a non-target, native species. Both species were subjected to each lampricide alone (TFM at species-specific 24 h LC10; niclosamide at 1.5% of [TFM]) or to a mixture of the two (sea lamprey at TFM 24 h LC10 + 1.5% niclosamide; bluegill at sea lamprey's TFM 24 h LC99.9 + 1.5% niclosamide) for 24 h. Tissues (brain, skeletal muscle, and liver) were sampled at 6, 12, and 24 h of exposure and assayed for whole tissue [ATP], [phosphocreatine (PCr)], [glycogen], [lactate], and [glucose]. In sea lamprey, TFM had little effect on brain and skeletal muscle, but niclosamide resulted in a depletion of high energy substrates in both tissues (brain ATP, PCr, glycogen, lactate, & glucose; muscle ATP, & glycogen). Sea lamprey exposed to the mixture showed general depletion of high energy substrates (brain ATP & glycogen; muscle ATP, PCr, & glycogen), accumulation of lactate, and high mortality rates. Bluegill were largely unaffected by exposure to either toxicant, alone or together, for the response endpoints measured. Our results indicate that lampricide toxicity in sea lamprey is mediated through a depletion of high energy substrates because of impaired aerobic ATP synthesis. We also confirmed that non-target bluegill show high tolerance to lampricide exposure, an effect potentially mediated through a high detoxification capacity relative to lampreys.