Center for Fisheries, Aquaculture, and Aquatic Sciences, Department of Zoology, Southern Illinois University, Carbondale, Illinois, 62901, USA.
Department of Entomology, Kansas State University, Manhattan, KS, 66506, USA.
Environ Pollut. 2021 Sep 1;284:117158. doi: 10.1016/j.envpol.2021.117158. Epub 2021 Apr 15.
Chronic exposure to pyrethroid insecticides can result in strong selective pressures on non-target species in aquatic systems and drive the evolution of resistance and population-level changes. Characterizing the underlying mechanisms of resistance is essential to better understanding the potential consequences of contaminant-driven microevolution. The current study found that multiple mechanisms enhance the overall tolerance of Hyalella azteca to the pyrethroid permethrin. In H. azteca containing mutations in the voltage-gated sodium channel (VGSC), both adaptation and acclimation played a role in mitigating the adverse effects of pyrethroid exposures. Pyrethroid resistance is primarily attributed to the heritable mutation at a single locus of the VGSC, resulting in reduced target-site sensitivity. However, additional pyrethroid tolerance was conferred through enhanced enzyme-mediated detoxification. Cytochrome P450 monooxygenases (CYP450) and general esterases (GE) significantly contributed to the detoxification of permethrin in H. azteca. Over time, VGSC mutated H. azteca retained most of their pyrethroid resistance, though there was some increased sensitivity from parent to offspring when reared in the absence of pyrethroid exposure. Permethrin median lethal concentrations (LC50s) declined from 1809 ng/L in parent (P) individuals to 1123 ng/L in the first filial (F) generation, and this reduction in tolerance was likely related to alterations in acclimation mechanisms, rather than changes to target-site sensitivity. Enzyme bioassays indicated decreased CYP450 and GE activity from P to F, whereas the VGSC mutation was retained. The permethrin LC50s in resistant H. azteca were still two orders-of-magnitude higher than non-resistant populations indicating that the largest proportion of resistance was maintained through the inherited VGSC mutation. Thus, the noted variation in tolerance in H. azteca is likely associated with inducible traits controlling enzyme pathways. A better understanding of the mechanistic and genomic basis of acclimation is necessary to more accurately predict the ecological and evolutionary consequences of contaminant-driven change in H. azteca.
慢性接触拟除虫菊酯杀虫剂会对水生系统中的非靶标物种产生强烈的选择压力，并导致抗药性的产生和种群水平的变化。描述抗药性的潜在机制对于更好地理解污染物驱动的微观进化的潜在后果至关重要。本研究发现，多种机制增强了食蚊鱼对拟除虫菊酯溴氰菊酯的整体耐受性。在含有电压门控钠离子通道（VGSC）突变的食蚊鱼中，适应和驯化都在减轻拟除虫菊酯暴露的不利影响方面发挥了作用。拟除虫菊酯抗性主要归因于 VGSC 单一基因座的遗传突变，导致靶位敏感性降低。然而，通过增强酶介导的解毒作用赋予了额外的拟除虫菊酯耐受性。细胞色素 P450 单加氧酶（CYP450）和一般酯酶（GE）显著促进了食蚊鱼中溴氰菊酯的解毒。随着时间的推移，VGSC 突变的食蚊鱼保留了大部分的拟除虫菊酯抗性，尽管在没有暴露于拟除虫菊酯的情况下饲养时，其从亲代到后代的敏感性略有增加。溴氰菊酯半数致死浓度（LC50）从亲代（P）个体的 1809ng/L 降至第一代（F）个体的 1123ng/L，这种耐度降低可能与驯化机制的改变有关，而不是靶位敏感性的改变。酶生物测定表明，从 P 到 F，CYP450 和 GE 的活性降低，而 VGSC 突变得以保留。抗性食蚊鱼的溴氰菊酯 LC50 仍比非抗性种群高出两个数量级，这表明通过遗传 VGSC 突变维持了最大比例的抗性。因此，食蚊鱼中耐受力的显著变化可能与控制酶途径的诱导特征有关。更好地理解驯化的机制和基因组基础对于更准确地预测食蚊鱼中污染物驱动变化的生态和进化后果是必要的。
