Aedes aegypti is responsible to the transmission of Dengue, Chikungunya and Zika virus in tropical and subtropical countries around the globe. In absence of vaccines or antivirals for human treatment, most control strategies are targeted to A. aegypti elimination. In the search for new compounds for mosquito control, α-aminonitriles, girgensohnine analogues were synthesized, these molecules showed inhibit acetylcholinesterase enzyme over insect’s vectors of diseases. However, α-aminonitriles AChE inhibition may not be the only mechanism of action of these molecules on insects. The aim of this work was to elucidate others α-aminonitriles targets as enzyme complexes of the mitochondrial electron-transport chain, the antioxidant activity to catalase and superoxide dismutase (SOD) on A. aegypti. Mitochondria were isolated from A. aegypti, stored in 2 mL eppendorf tubes at -70 °C and fragmented using ultrasound for 10 min. Complexes of mitochondrial electron-transport chain, antioxidant activity to catalase and superoxide dismutase (SOD) using concentrations 8nM, 2 μM, 8 μM and 40 μM of the four compounds with the highest insecticide activity were evaluated. Results indicated that analogs caused significant inhibition of enzyme activity between 12 and 44% on the complex I (NADH dehydrogenase) and oxidase succinate from 20 to 44% in the electron transport chain. The succinate dehydrogenase activity increased from 65 to 162%, as the values of cytochrome c oxidase which varied from 28 to 106%. It was found that the compounds caused inhibition of the catalase, preventing the reduction of H₂O₂ that can induce the formation of EROS. The compounds tested showed effect on complex I by blocking the release of electrons, promoting and encouraging the formation of EROS in the mitochondria.