Since the 1960s, chemical control of larval sea lamprey has been achieved using the pesticides 3-trifluoromethyl-4-nitrophenol (TFM) and niclosamide (Bayluscide). Much more potent, niclosamide is often used as an adjuvant for TFM, and on its own to treat lentic habitats, rivers with high discharge and currents, and for population surveys. Yet, little is known about its mode of action or physiological effects on sea lamprey. Like TFM, niclosamide is thought to impair mitochondrial ATP production by uncoupling oxidative phosphorylation. We therefore tested the hypothesis that niclosamide would result in metabolic perturbations and disturbances to acid-base balance in larval lamprey, due to their need to balance ATP supply with ATP demands. When larval sea lamprey was exposed to the nominal 9-h niclosamide LC₅₀ (0.11 mg L⁻¹) over 9 h, it resulted in significant decreases in brain ATP (33%), phosphocreatine (35%) and glycogen (50%), accompanied by a 5-fold increase in lactate. In carcass, there were 25-30 % decreases in glycogen, corresponding increases in pyruvate and lactate, and a pronounced, 0.5 unit decrease in intracellular pH. Calculation of the NAD⁺/NADH ratio in the carcass indicated that neither oxygen delivery nor the flux of reducing equivalents through the mitochondrial electron transport chain were impaired by niclosamide, supporting the hypothesis that niclosamide interferes with mitochondrial ATP production by uncoupling oxidative phosphorylation. Thus, greater reliance on glycogen, characterized by higher rates of glycolysis, temporarily mitigates the corresponding shortfall in ATP supply caused by niclosamide. Notably, all lamprey that survived niclosamide exposure readily restored ATP, phosphocreatine, glycogen and acid-base balance after recovery in niclosamide-free water. This resilience suggests that sea lamprey that survive or escape niclosamide treatment could compromise sea lamprey control efforts by subsequently completing their larval stage and developing into parasitic juvenile sea lamprey that could ultimately threaten Great Lake's fisheries populations.

自 1960 年代以来，已使用杀虫剂 3-三氟甲基-4-硝基苯酚 (TFM) 和氯硝柳胺 (Bayluscide) 实现对海鳗幼体的化学防治。更有效的是，氯硝柳胺通常用作 TFM 的佐剂，并单独用于治疗静息栖息地、高流量和水流的河流以及人口调查。然而，人们对其作用方式或对海七鳃鳗的生理影响知之甚少。与 TFM 一样，氯硝柳胺被认为通过解偶联氧化磷酸化来损害线粒体 ATP 的产生。因此，我们测试了氯硝柳胺会导致幼虫七鳃鳗的代谢紊乱和酸碱平衡紊乱的假设，因为它们需要平衡 ATP 供应和 ATP 需求。当幼体海七鳃鳗暴露于标称的 9 小时氯硝柳胺 LC ₅₀(0.11 mg L ^-1 ) 超过 9 小时，导致脑 ATP (33%)、磷酸肌酸 (35%) 和糖原 (50%) 显着下降，同时乳酸增加 5 倍。在胴体中，糖原减少 25-30%，丙酮酸和乳酸相应增加，细胞内 pH 值显着降低 0.5 个单位。计算 NAD ⁺胴体中的 /NADH 比值表明，氯硝柳胺既不会损害氧气输送，也不会损害通过线粒体电子传递链的还原当量通量，这支持了氯硝柳胺通过解偶联氧化磷酸化干扰线粒体 ATP 产生的假设。因此，以更高的糖酵解速率为特征的对糖原的更大依赖暂时缓解了由氯硝柳胺引起的相应的 ATP 供应短缺。值得注意的是，所有在氯硝柳胺暴露中幸存下来的七鳃鳗在不含氯硝柳胺的水中恢复后都容易恢复 ATP、磷酸肌酸、糖原和酸碱平衡。