How does a mouse die from poison? - briefly
The poison disrupts essential biological functions, causing swift failure of the nervous or cardiovascular systems and resulting in death within minutes to hours depending on the dose and compound. Typical outcomes include paralysis, respiratory collapse, and cardiac arrest.
How does a mouse die from poison? - in detail
When a rodent consumes a toxic compound, the substance enters the gastrointestinal tract, is absorbed into the bloodstream, and circulates to target organs. The specific pathway to death depends on the chemical class of the poison.
Anticoagulant rodenticides (e.g., warfarin, brodifacoum) block vitamin K‑dependent clotting factors. Blood loss begins several hours after ingestion, initially unnoticed because clotting remains partially functional. As factor levels fall below critical thresholds, spontaneous hemorrhages appear in the lungs, brain, and gastrointestinal lining. Internal bleeding leads to hypovolemic shock, loss of perfusion, and ultimately cardiac arrest.
Neurotoxic agents (e.g., bromethalin, strychnine) interfere with neuronal signaling. Bromethalin uncouples mitochondrial oxidative phosphorylation, causing cerebral edema and seizures. Strychnine antagonizes glycine receptors in the spinal cord, producing uncontrolled muscle contractions and respiratory paralysis. The resulting respiratory failure produces rapid hypoxia and cardiac arrest within minutes to a few hours.
Metabolic poisons (e.g., zinc phosphide, phosphine gas) generate toxic gases in the acidic stomach environment. Phosphine disrupts cellular respiration by inhibiting cytochrome c oxidase, leading to systemic energy failure. Organs with high oxygen demand—heart, brain, kidneys—experience acute necrosis. Multi‑organ failure ensues, typically within 12–24 hours.
Metallic salts (e.g., arsenic, copper sulfate) bind sulfhydryl groups in enzymes, halting critical metabolic pathways. Cellular apoptosis spreads from the liver to the central nervous system. Clinical signs include vomiting, diarrhea, and severe dehydration, culminating in circulatory collapse.
The progression from ingestion to death follows a predictable sequence: absorption → distribution → target organ interaction → physiological disruption → loss of vital function. The time frame varies with dosage, poison potency, and the animal’s health status, ranging from minutes (high‑dose neurotoxins) to several days (low‑dose anticoagulants). Ultimately, the lethal outcome results from irreversible failure of one or more essential organ systems.