ROS-Mediated <i>COXI</i> Overexpression by AMPKα Confers Resistance to Dimefluthrin and Cross-Resistance to Indoxacarb in <i>Aedes albopictus</i>

Increased electron respiratory chain complex and Na⁺, K⁺-ATPase activity, ROS content, <i>COXI</i> and <i>AMPKα</i> expression, and decreased free ATP content were detected in a dimefluthrin-resistant <i>Aedes albopictus</i> (<i>Ae. albopictus</i>) strain established in laboratory, which developed high-level resistance to dimefluthrin and cross-resistance to indoxacarb and the resistance ratio of 21.61- and 62.14-fold shifted to 8.69- and 8.00-fold to dimefluthrin and indoxacarb after silencing <i>COXI</i>. When silencing <i>AMPKα</i>, the ROS content increased by 1.74 times and the expression of <i>COXI</i> was decreased by 59.00%, leading to a significant increase in the susceptibility of resistant <i>Ae. albopictus</i> to dimefluthrin. Removing ROS by <i>N</i>-acetylcysteine remarkably decreased the expression of <i>AalAMPKα</i>, restored the expression of <i>COXI</i>, and significantly increased the mortality of resistant <i>Ae. albopictus</i> when exposed to dimefluthrin and indoxacarb, suggesting that <i>COXI</i> played a crucial role in mediating the resistance to dimefluthrin and indoxacarb by modulating <i>AalAMPKα</i> expression. The study showed that dimefluthrin triggered the outbreak of ROS, subsequently modulated the expression of <i>COXI</i>, and as a result induced the <i>AalAMPKα</i>-mediated resistance to insecticides targeted voltage-gated sodium channel.