Increasing evidence suggests that phenotypic plasticity can play a critical role in ecotoxicology. More specifically, induced pesticide tolerance, in which populations exposed to a contaminant show increased tolerance to the contaminants later, has been documented in multiple taxa. However, the physiological mechanisms of induced tolerance remain unclear. We hypothesized that induced pesticide tolerance is the result of a generalized stress response based on previous studies showing that both natural stressors and anthropogenic stressors can induce tolerance to pesticides. We tested this hypothesis by first exposing larval wood frogs (Rana sylvatica) to either an anthropogenic stressor (sublethal carbaryl concentration), a natural stressor (cues from a caged predator), or a simulated stressor via exogenous exposure to the stress hormone corticosterone (125 nM). We also included treatments that inhibited corticosterone synthesis with the compound metyrapone (MTP). We then exposed the larvae to a lethal carbaryl treatment to assess time to death. We found that prior exposure to 125 nM of exogenous CORT and predator cues induced tolerance to a lethal concentration of carbaryl through a slight delay in time to death. Pre-exposure to sublethal carbaryl, as well as MTP alone or in combination with predator cues, did not induce tolerance to the lethal carbaryl concentration relative to the ethanol vehicle control treatment. Our study provides evidence that pesticide tolerance can be induced by a generalized stress response both in the presence and absence (exogenous CORT) of specific cues and highlights the importance of considering physiological ecology and environmental context in ecotoxicology.

越来越多的证据表明，表型可塑性可以在生态毒理学中发挥关键作用。更具体地说，诱导的杀虫剂耐受性已被记录在多个分类群中，其中接触污染物的种群后来显示出对污染物的更高的耐受性。但是，诱导耐受的生理机制仍不清楚。我们基于先前的研究假设诱导的农药耐受性是广义胁迫反应的结果，该研究表明自然胁迫和人为胁迫均可以诱导对农药的耐受性。我们通过首先暴露幼虫木蛙（Rana sylvatica），或者通过外源性暴露于应激激素皮质酮（125 nM）暴露于人为应激源（亚甲萘威浓度达到致命性），自然应激源（笼养捕食者的提示）或模拟应激源。我们还包括了用复方甲吡酮（MTP）抑制皮质酮合成的治疗方法。然后，我们将幼虫暴露于致命的甲萘威治疗中以评估死亡时间。我们发现，事先暴露于125 nM的外源CORT和捕食者线索会导致死亡时间略微延迟，从而导致对甲萘威的致死浓度具有耐受性。相对于乙醇媒介物对照处理，预先暴露于亚致死甲萘芳基以及单独使用MTP或与捕食者线索结合使用均未引起对致死甲萘芳基浓度的耐受性。