How does SES poison fleas? - briefly
SES functions as a neurotoxic insecticide that binds to acetylcholinesterase in fleas, blocking nerve signal termination and causing uncontrolled muscle activity leading to rapid death. The chemical penetrates the flea’s cuticle and reaches the central nervous system within minutes.
How does SES poison fleas? - in detail
The SES formulation acts as a neurotoxic agent that interferes with flea physiology at several points. Upon contact, the compound penetrates the cuticle and enters the hemolymph, where it binds to voltage‑gated sodium channels in neuronal membranes. Binding forces the channels to remain open, causing uncontrolled sodium influx, depolarization, and rapid loss of nerve impulse control. The resulting paralysis halts locomotion and feeding, leading to death within minutes.
In parallel, SES disrupts mitochondrial respiration. The chemical inhibits complex III of the electron transport chain, reducing ATP production and generating reactive oxygen species. Energy depletion compromises muscle contraction and metabolic homeostasis, accelerating fatal outcomes.
The toxic cascade proceeds as follows:
- Cuticular absorption within seconds.
- Distribution through hemolymph to nervous tissue.
- Sodium‑channel activation → continuous depolarization.
- Mitochondrial inhibition → ATP shortage, oxidative stress.
- Systemic paralysis and cessation of vital functions.
Dose‑response data indicate a median lethal concentration (LC₅₀) of approximately 0.12 µg cm⁻² for adult fleas under laboratory conditions. Sublethal exposure still impairs reproduction by affecting oocyte development, contributing to population control.
Resistance mechanisms, when observed, involve up‑regulation of detoxifying enzymes such as cytochrome P450 mono‑oxygenases, which metabolize the active moiety before it reaches neural targets. Countermeasures include rotating SES with agents that have distinct modes of action to prevent enzyme‑mediated adaptation.