Selective toxicity and molecular disruption induced by acetamiprid in the predator, Cyrtorhinus lividipennis Reuter (Hemiptera: Miridae).

This study investigates the selective toxicity and molecular interactions of acetamiprid (ACE) with the predator Cyrtorhinus lividipennis and calf thymus DNA (ctDNA). The selective ratio (SR) of ACE was (SR ≤ 1), 0.564 and 0.513 after 24 and 48 respectively, indicating non-selectivity and higher toxicity to C. lividipennis than to the target pest Nilaparvata lugens. Sublethal concentrations (LC10 and LC30) of ACE exhibited concentration- and time-dependent effects on C. lividipennis, including increased mortality. Biochemical analysis revealed metabolic stress in C. lividipennis, along with increased activity of antioxidant enzymes. DNA damage was assessed using the comet assay, showing significant increases in tail length at both LC10 and LC30, indicating considerable DNA fragmentation. Histological analysis revealed a dose-dependent response to ACE in C. lividipennis, with midgut tissue damage becoming progressively more severe at the LC30 concentration. Biophysical techniques, including UV-visible absorption and fluorescence spectroscopy, demonstrated that ACE binds to ctDNA, primarily via groove binding, as confirmed by displacement assays with Hoechst 33258 and ethidium bromide (EtBr). The binding constant (Kb) and Stern-Volmer analysis indicated moderate to high binding affinity with a stable ACE-ctDNA complex formed through non-covalent interactions. Molecular docking revealed that ACE interacts with ctDNA via hydrogen bonds and van der Waals forces, stabilizing the complex within the minor groove. Collectively, these results highlight the selective toxicity of ACE to pest species while posing potential risks to beneficial organisms and causing significant molecular and physiological damage.