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 (P₀) individuals to 1123 ng/L in the first filial (F₁) 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 P₀ to F₁, 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.

长期暴露于拟除虫菊酯类杀虫剂会导致对水生系统中非目标物种的强大选择性压力，并推动耐药性和种群水平变化的演变。表征抗药性的基本机制对于更好地理解污染物驱动的微进化的潜在后果至关重要。当前的研究发现多种机制增强了透明质酸对拟除虫菊酯苄氯菊酯的总体耐受性。在阿兹台克人由于在电压门控钠通道（VGSC）中含有突变，因此适应性和适应性在减轻拟除虫菊酯暴露的不利影响中发挥了作用。拟除虫菊酯抗药性主要归因于VGSC单个基因座的可遗传突变，从而导致靶位点敏感性降低。然而，通过增强的酶介导的排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）显着促进了阿兹台克人中氯菊酯的解毒。随着时间的流逝，VGSC突变了阿兹台克人H. azteca保留了大部分对拟除虫菊酯的抗性，尽管在没有拟除虫菊酯暴露的情况下饲养时，父母对后代的敏感性有所提高。苄氯菊酯中位致死浓度（LC50s）从亲本（P ₀）个体的1809 ng / L下降到第一代孝子（F ₁）的1123 ng / L ，这种耐受性的降低很可能与适应机制的改变有关，相反而不是改变目标位置的灵敏度。酶生物测定表明CYP450和GE活性从P _0降低至F ₁，而VGSC突变得以保留。苄氯菊酯LC50s在抗性阿兹台克人中仍然比非抗性种群高两个数量级，表明通过遗传的VGSC突变维持了最大比例的抗性。因此，阿兹台克人的耐受性的显着变化很可能与控制酶途径的诱导性状有关。为了更准确地预测阿兹台克人由污染物引起的变化的生态和进化后果，必须更好地了解适应的机理和基因组学基础。