Mitochondria-targeted nanocarriers doubled the toxicity of oxidative phosphorylation and ATP synthesis disruptive insecticides against Spodoptera frugiperda

Translocation and delivery of pesticides onto the molecular target is often a limiting step of efficacy, causing excessive use of pesticides and adverse effects on the environment and human health. Advances of nanomaterials have opened up a new avenue for effective translocation and delivery to increase the pesticide efficacy and reduce risks. We successfully synthesized and fully characterized a mesoporous silica nanoparticle-based mitochondria-targeted pesticide nanocarrier for the oxidative phosphorylation and ATP synthesis disruptor chlorfenapyr (Chl). The nanocarriers can be readily absorbed orally and translocated into the midgut and Malpighian duct of Spodoptera frugiperda larvae and target mitochondria at the subcellular level. The Chl loading content on the nanocarrier was up to 35%. The toxicity of the Chl nanocarriers to the 3rd instar S. frugiperda larvae (half-maximum lethal concentration (LC50), 16.4 mu g g(-1) expressed by the Chl content) was almost doubled relative to Chl alone (LC50 = 30.1 mu g g(-1)). Further research showed that the mitochondria-targeted nanocarrier enhanced Chl efficacy by inducing mitochondrial damage in Sf9 cells, which led to the collapse of the mitochondrial membrane potential and reduction of ATP production. The mitochondria-targeted nanocarriers have great application potential in the formulation of oxidative phosphorylation and ATP synthesis disruptors, which can minimize their potential threats to food/environmental safety.

Automated summary

The translocation and delivery of pesticides to their target molecules is often a limiting factor in their efficacy. Nanomaterials have provided a new approach to increase pesticide efficacy and reduce risks. In this study, a mitochondria-targeted pesticide nanocarrier was successfully synthesized, which enhanced the toxicity and efficacy of the pesticide chlorfenapyr by inducing mitochondrial damage.