Department of Biology, Wilfrid Laurier University and the Laurier Institute for Water Science, 75 Universtiy Avenue West, Waterloo, Ontario N2L 3C5, Canada.
Department of Biology, Wilfrid Laurier University and the Laurier Institute for Water Science, 75 Universtiy Avenue West, Waterloo, Ontario N2L 3C5, Canada.
Ecotoxicol Environ Saf. 2022 Jan 1;229:112969. doi: 10.1016/j.ecoenv.2021.112969. Epub 2021 Dec 16.
Since the 1960s, invasive sea lamprey (Petromyzon marinus) populations in the Laurentian Great Lakes have been controlled by applying two chemicals, 3-trifluoromethyl-4-nitrophenol (TFM) and 2',5-dichloro-4'-nitrosalicylanilide (niclosamide, aka. Bayluscide®), to streams infested with larval sea lamprey. These "lampricide" applications primarily rely on TFM, and are often combined with 1-2% niclosamide, which increases treatment effectiveness. Niclosamide is also used alone to treat lentic habitats and in rivers with high discharge. However, little is known about niclosamide's possible adverse physiological effects on non-target organisms. Of particular concern is the lake sturgeon (Acipenser fulvescens), which is threatened throughout the Great Lakes basin where its habitat often overlaps with larval lamprey. Because niclosamide is believed to impair ATP production by uncoupling oxidative phosphorylation, we determined how it altered metabolic processes and acid-base balance in young-of-the-year (YOY) lake sturgeon exposed to their 9-h LC of niclosamide (0.11 mg L) for 9 h. Exposure to niclosamide led to decreased brain ATP and glucose reserves, and increased lactate, with no effect on brain glycogen. In contrast, substantial (60%) reductions in glycogen were observed in liver, suggesting that hepatic glycogen reserves were mobilized to meet the brain's glucose requirements when ATP supply was impaired during niclosamide exposure. Disturbances in carcass included reduced phosphocreatine (65-70%), 2- and 4-fold increases in pyruvate and lactate, and a slight metabolic acidosis, characterized by a 0.1 unit decrease in intracellular pH (pHi). Each of these disturbances were corrected within 24 h following depuration in clean (niclosamide-free) water. We conclude that if lake sturgeon survive exposure to niclosamide, they are able to rapidly replenish their energy stores (glycogen, ATP, phosphocreatine) and correct any corresponding metabolic disturbances within 24 h.
自 20 世纪 60 年代以来，通过在受幼虫海七鳃鳗感染的溪流中施用两种化学物质——3-三氟甲基-4-硝基苯酚（TFM）和 2'，5-二氯-4'-硝基亚水杨酰胺（氯硝柳胺，又名 Bayluscide®），来控制大湖区的入侵性海七鳃鳗种群。这些“杀海七鳃鳗剂”的应用主要依赖于 TFM，并经常与 1-2%的氯硝柳胺结合使用，这可以提高治疗效果。氯硝柳胺也单独用于治疗静水池生境和排放量大的河流。然而，人们对氯硝柳胺对非目标生物可能产生的不良生理影响知之甚少。特别令人关注的是湖鲟（Acipenser fulvescens），它在大湖区受到威胁，其栖息地经常与幼虫海七鳃鳗重叠。由于氯硝柳胺被认为通过解偶联氧化磷酸化来破坏 ATP 的产生，因此我们确定了它如何改变暴露于其 9 小时 LC（0.11mg/L）氯硝柳胺 9 小时的幼年湖鲟的代谢过程和酸碱平衡。暴露于氯硝柳胺导致大脑 ATP 和葡萄糖储备减少，乳酸增加，而对大脑糖原没有影响。相比之下，在肝脏中观察到大量（60%）的糖原减少，这表明当氯硝柳胺暴露时 ATP 供应受损时，肝糖原储备被动员以满足大脑的葡萄糖需求。鱼体组织的紊乱包括磷酸肌酸减少（65-70%）、丙酮酸和乳酸增加 2-4 倍，以及轻微的代谢性酸中毒，表现为细胞内 pH（pHi）降低 0.1 个单位。在清洁（无氯硝柳胺）水中进行净化后，这些紊乱中的每一个都在 24 小时内得到纠正。我们的结论是，如果湖鲟能够在接触氯硝柳胺后存活下来，它们能够在 24 小时内迅速补充能量储备（糖原、ATP、磷酸肌酸），并纠正任何相应的代谢紊乱。
