How does poison work on rats? - briefly
Poison disrupts essential physiological pathways—anticoagulants inhibit vitamin K recycling, causing uncontrolled internal bleeding, while neurotoxins block acetylcholine receptors, leading to paralysis and respiratory failure. The resulting organ dysfunction rapidly culminates in death.
How does poison work on rats? - in detail
Rodent toxicants act through specific biochemical pathways that interrupt vital physiological processes. After ingestion, the compound is absorbed through the gastrointestinal tract, enters the bloodstream, and reaches target organs. The lethal effect depends on the chemical class, dose, and the animal’s metabolic capacity.
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Anticoagulant agents (e.g., warfarin, brodifacoum) block vitamin K epoxide reductase, preventing regeneration of active vitamin K. This stops the carboxylation of clotting factors II, VII, IX, and X, leading to uncontrolled hemorrhage. Clinical signs appear 2–5 days after exposure, with internal bleeding as the primary cause of death.
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Neurotoxic phosphides (zinc phosphide, aluminum phosphide) react with stomach acid to release phosphine gas. Phosphine interferes with mitochondrial cytochrome c oxidase, halting ATP production and causing rapid cellular necrosis. Symptoms include respiratory distress, seizures, and sudden collapse within hours.
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Metabolic disruptors such as bromethalin inhibit mitochondrial oxidative phosphorylation by uncoupling electron transport. Energy failure leads to cerebral edema and paralysis. Onset is delayed, typically 24–72 hours, with progressive loss of coordination and eventual respiratory failure.
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Vitamin D analogs (cholecalciferol) raise serum calcium by enhancing intestinal absorption and bone resorption. Hypercalcemia triggers renal failure, cardiac arrhythmia, and vascular calcification. Mortality occurs 3–5 days post‑exposure, preceded by polyuria, lethargy, and muscle weakness.
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Phosphonic acid derivatives (sodium monofluoroacetate) convert to fluorocitrate, which blocks the aconitase step of the citric‑acid cycle. Energy production stalls, causing convulsions and cardiac arrest within 12–24 hours.
Resistance mechanisms include up‑regulated vitamin K recycling enzymes for anticoagulants and enhanced detoxification pathways for bromethalin. Secondary poisoning risk is low for anticoagulants due to rapid metabolism in predators, but phosphine and bromethalin can affect non‑target species if ingested in large amounts.
Effective control relies on selecting a toxicant whose mode of action matches the target population’s susceptibility, applying an appropriate dose (typically 0.1–0.5 mg kg⁻¹ for anticoagulants, 2–5 mg kg⁻¹ for bromethalin), and monitoring for delayed mortality. Proper bait placement and environmental safeguards minimize accidental exposure and reduce the likelihood of resistance development.