Population control of invasive sea lamprey relies heavily on lampricide treatment of infested streams. The lampricide 3-trifluoromethyl-4-nitrophenol (TFM) is thought to impair mitochondrial ATP production through uncoupling oxidative phosphorylation. However, the effect of TFM on the entire electron transport chain (complexes I to V) in the mitochondria is not clear. In addition, TFM is reduced in phase I metabolism by sea lamprey at higher levels than in other fish species. The effects of these TFM reductive metabolites on mitochondria have not been explored. In this study, we sought to examine the effects of TFM and its reductive metabolite amino-TFM (TFMa) on cardiac mitochondrial oxygen consumption and membrane potential to delineate potential mechanisms for toxicity. To determine if molecules with similar structure also exhibit similar effects on mitochondria, we used 4-nitro-3-methylphenol (NMP) and its reductive metabolites 4-amino-3-methylphenol (NMPa) and 4-nitroso-3-methylphenol (NMPn) for comparisons. We found that mitochondrial bioenergetics was heavily affected with increasing concentrations of TFM, NMP, and NMPa when complexes I and II of the electron transport chain were examined, indicating that the toxic action of these compounds was exerted not only by uncoupling complex V, but also affecting complexes I and II.

中文翻译：

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暴露于TFM及其代谢产物后，海鳗的心脏线粒体生物能。

侵袭性海七rey鳗的种群控制在很大程度上依赖于对被侵染的溪流进行杀虫剂处理。灭光剂3-三氟甲基-4-硝基苯酚（TFM）被认为通过解偶联氧化磷酸化而损害线粒体ATP的产生。然而，尚不清楚TFM对线粒体中整个电子传输链（复合物I至V）的影响。此外，与其他鱼类相比，海蓝rey在第一阶段的新陈代谢中降低了TFM的含量。这些TFM还原性代谢物对线粒体的影响尚未探索。在这项研究中，我们试图检查TFM及其还原性代谢物氨基TFM（TFMa）对心脏线粒体耗氧量和膜电位的影响，以描述潜在的毒性机制。为了确定结构相似的分子是否对线粒体也表现出相似的作用，我们使用了4-硝基-3-甲基苯酚（NMP）及其还原性代谢物4-氨基-3-甲基苯酚（NMPa）和4-硝基--3-甲基苯酚（NMPn ）进行比较。我们发现当检查电子传输链的配合物I和II时，随着TFM，NMP和NMPa浓度的增加，线粒体生物能学受到严重影响，这表明这些化合物的毒性作用不仅是通过解偶联复合物V而发挥的，而且影响复合体I和II。