How does cypermethrin act on bedbugs? - briefly
Cypermethrin, a synthetic pyrethroid, binds to voltage‑gated sodium channels in the insect nervous system, prolonging channel opening and causing uncontrolled nerve firing. This hyperexcitation produces paralysis and rapid death of bedbugs.
How does cypermethrin act on bedbugs? - in detail
Cypermethrin, a synthetic pyrethroid, targets the nervous system of Cimex lectularius by binding to voltage‑gated sodium channels on neuronal membranes. The compound stabilizes the open conformation of these channels, preventing rapid inactivation. Sustained sodium influx generates prolonged depolarization, producing repetitive firing of nerve impulses. This hyperexcitation manifests as tremors, loss of coordination, and ultimately paralysis (knock‑down effect).
After topical exposure, cypermethrin penetrates the insect cuticle primarily through lipid pathways. Once inside the hemocoel, it distributes via the hemolymph to the central nervous system. The toxin’s lipophilicity ensures accumulation in neuronal tissue, where it exerts its action at micromolar concentrations. Lethal dose (LD₅₀) values for adult bedbugs range from 0.05 to 0.2 µg per insect, reflecting high potency.
Metabolic detoxification pathways in bedbugs involve cytochrome P450 enzymes, esterases, and glutathione‑S‑transferases. Up‑regulation of these enzymes reduces internal toxin concentration, contributing to resistance. Additionally, point mutations in the para‑sodium channel gene (kdr mutations) alter the binding site, decreasing affinity for cypermethrin and mitigating its neurotoxic effect.
Formulation factors influence efficacy:
- Carrier solvents (e.g., isoparaffins) enhance cuticular absorption.
- Adjuvants (e.g., surfactants) reduce surface tension, improving coverage.
- Residual activity depends on substrate type; porous materials retain less active ingredient than smooth surfaces.
Synergistic use with other classes (e.g., neonicotinoids or organophosphates) can overcome metabolic resistance by inhibiting detoxification enzymes, resulting in higher mortality rates.
In summary, cypermethrin induces rapid neuronal depolarization through sodium‑channel modulation, leading to paralysis and death. Resistance arises from both target‑site mutations and enhanced metabolic clearance, while formulation characteristics determine the practical field performance against bedbugs.