How does poison affect rats? - briefly
Poison disrupts essential biochemical processes, producing convulsions, respiratory failure, and rapid organ collapse that culminates in death.
How does poison affect rats? - in detail
Toxic agents disrupt rat physiology through absorption, distribution, metabolism, and excretion. After ingestion, inhalation, or dermal contact, the compound enters the bloodstream and reaches target organs. The severity of the response depends on the chemical class, dose, and exposure route.
Acute poisoning typically produces rapid onset of neurological, cardiovascular, and gastrointestinal signs. Common manifestations include:
- Tremors, convulsions, or loss of coordination
- Respiratory distress or apnea
- Salivation, vomiting, and diarrhea
- Bradycardia or tachycardia
- Hypotension or hypertension
Sub‑lethal exposure may cause chronic effects such as organ degeneration, reproductive impairment, and altered behavior. Specific mechanisms vary by poison type:
- Anticoagulants (e.g., warfarin, brodifacoum) – inhibit vitamin K recycling, preventing clotting factor synthesis; result is internal hemorrhage.
- Neurotoxins (e.g., strychnine, organophosphates) – block inhibitory neurotransmission or inhibit acetylcholinesterase; lead to uncontrolled muscle activity and respiratory failure.
- Metabolic poisons (e.g., metal phosphides, cyanide) – interfere with cellular respiration; cause rapid energy collapse and tissue hypoxia.
- Rodenticides containing zinc phosphide – release phosphine gas in the stomach; phosphine binds to cytochrome c oxidase, halting oxidative phosphorylation.
- Heavy metals (e.g., lead, mercury) – accumulate in kidneys and brain; provoke oxidative stress, enzyme inhibition, and neurobehavioral deficits.
Dose–response relationships are quantified by LD₅₀ values, indicating the amount required to kill 50 % of a test population. For most anticoagulants, LD₅₀ ranges from 20 mg/kg to 200 mg/kg; neurotoxins often have LD₅₀ below 1 mg/kg, reflecting higher potency.
Metabolic pathways determine toxin clearance. Hepatic enzymes such as cytochrome P450 oxidize many organic poisons, producing metabolites that may be more or less toxic. Renal excretion eliminates water‑soluble derivatives; failure of these systems accelerates mortality.
Behavioral changes precede physiological collapse. Affected rats display reduced locomotion, grooming deficits, and altered feeding patterns, providing early indicators for toxicological assessment.
Effective control relies on selecting agents with appropriate toxicity profiles, ensuring rapid onset of lethal action while minimizing secondary exposure to non‑target species. Continuous monitoring of symptom progression and post‑mortem tissue analysis confirm cause of death and inform mitigation strategies.