How does mouse poison work? - briefly
Mouse baits contain anticoagulant chemicals (e.g., bromadiolone, warfarin) that inhibit vitamin K recycling, preventing blood clotting and causing internal bleeding that kills the rodent within days. Other formulations employ neurotoxins that impair nerve signaling, leading to rapid paralysis and respiratory failure.
How does mouse poison work? - in detail
Rodent toxicants act by introducing chemicals that disrupt vital physiological processes. Most products contain one of several active agents, each with a specific mode of action.
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Anticoagulant compounds (e.g., warfarin, brodifacoum) inhibit vitamin K epoxide reductase, preventing the regeneration of active vitamin K. Without functional vitamin K, clotting factors II, VII, IX, and X cannot be carboxylated, leading to progressive internal bleeding. Effects appear after 24–72 hours, allowing the animal to consume a lethal dose before symptoms manifest.
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Neurotoxicants such as bromethalin interfere with mitochondrial oxidative phosphorylation. The compound uncouples electron transport, causing rapid depletion of ATP in neuronal cells. Energy failure results in paralysis, convulsions, and death within a few hours.
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Calcium‑based agents (cholecalciferol, i.e., vitamin D₃) raise serum calcium by enhancing intestinal absorption and bone resorption. Hypercalcemia triggers renal failure, cardiac arrhythmias, and vascular calcification. Mortality typically occurs after several days of exposure.
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Metal phosphides (zinc phosphide) react with stomach acid to release phosphine gas. Phosphine penetrates cellular membranes, inhibiting cytochrome c oxidase and halting aerobic respiration. Acute respiratory distress and multi‑organ failure follow within minutes to hours.
Absorption routes include oral ingestion of bait, dermal contact with contaminated surfaces, and, in rare cases, inhalation of volatilized gases. After entry, the toxin distributes via the bloodstream to target organs, where it binds to specific enzymes or receptors. Metabolic pathways either activate pro‑toxins (as with phosphides) or detoxify compounds; resistance can develop when rodents up‑regulate hepatic enzymes that neutralize anticoagulants.
Symptoms reflect the underlying biochemical disruption: internal hemorrhage, neurological impairment, electrolyte imbalance, or respiratory collapse. Diagnosis relies on observation of clinical signs combined with knowledge of the toxin used. Treatment options are limited; anticoagulant poisoning may be countered with high‑dose vitamin K₁, while other agents lack specific antidotes and require supportive care.
Safety measures include placing bait in tamper‑proof stations, using formulations with delayed action to reduce secondary poisoning, and rotating active ingredients to prevent resistance. Proper disposal of dead rodents and contaminated materials minimizes environmental exposure.