How does benzyl benzoate act on a tick? - briefly
Benzyl benzoate penetrates the tick’s cuticle, accumulates in the nervous system, and blocks octopamine‑mediated signaling, causing paralysis and death. Its rapid action makes it effective for topical acaricidal treatments.
How does benzyl benzoate act on a tick? - in detail
Benzyl benzoate penetrates the tick’s exoskeleton by dissolving lipids in the cuticle, allowing rapid entry into internal tissues. Once inside, the compound interferes with neuronal transmission by disrupting the function of voltage‑gated sodium channels, leading to uncontrolled firing and paralysis. The resulting loss of coordination prevents the tick from attaching to the host and halts feeding.
The toxic effect is amplified by inhibition of mitochondrial respiration. Benzyl benzoate uncouples oxidative phosphorylation, reducing ATP synthesis and causing energy depletion. Cellular swelling follows, damaging gut epithelium and respiratory tissues, which accelerates mortality.
Key pharmacodynamic features include:
- Lipophilicity – high affinity for the tick’s waxy cuticle ensures efficient absorption.
- Neurotoxicity – blockage of sodium channel gating produces rapid paralysis.
- Metabolic disruption – uncoupling of mitochondrial membranes leads to systemic failure.
Resistance is uncommon because the mechanism targets multiple essential pathways. However, prolonged sub‑lethal exposure can select for cuticle thickening or altered enzyme expression, underscoring the need for correct dosage.
In practice, benzyl benzoate is applied as a topical solution or incorporated into acaricidal formulations. Proper concentration (typically 25 %–50 % w/v) delivers lethal doses within hours, while lower concentrations serve as repellents by irritating sensory receptors on the tick’s tarsal organs.
Overall, the compound’s dual action—neuroparalysis combined with metabolic collapse—provides a rapid and effective means of eliminating ticks.