How does poison affect mice? - briefly
Poison disrupts essential biochemical processes, causing swift organ failure and, at lethal concentrations, death. Symptoms emerge within minutes to hours, varying with the toxin’s mode of action and dose.
How does poison affect mice? - in detail
Poison exposure in rodents follows a predictable sequence of absorption, distribution, metabolism, and elimination that determines the severity and pattern of toxicity. After ingestion, inhalation, or dermal contact, the compound enters the bloodstream and reaches target organs such as the liver, kidneys, heart, and central nervous system. Metabolic enzymes, primarily hepatic cytochrome P450 isoforms, can convert the parent toxin into more reactive metabolites, which may bind cellular macromolecules and trigger oxidative stress, mitochondrial dysfunction, or enzyme inhibition.
The dose–response relationship governs clinical outcomes. Sub‑lethal doses typically produce transient signs—hypoactivity, tremor, salivation, or mild gastrointestinal irritation—while higher concentrations lead to convulsions, respiratory depression, cardiac arrhythmia, and rapid mortality. Specific toxins exhibit characteristic organotropism:
- Neurotoxins (e.g., organophosphates, tetrodotoxin): block acetylcholinesterase or sodium channels, causing muscle fasciculations, paralysis, and respiratory failure.
- Hepatotoxins (e.g., carbon tetrachloride, acetaminophen): generate free radicals, resulting in centrilobular necrosis, elevated transaminases, and coagulopathy.
- Nephrotoxins (e.g., heavy metals, cisplatin): accumulate in proximal tubules, producing tubular necrosis, oliguria, and electrolyte imbalance.
- Cardiotoxins (e.g., digitalis glycosides, certain alkaloids): disrupt ion homeostasis, leading to bradyarrhythmia or ventricular tachycardia.
Pathophysiological effects progress through three phases. The initial phase involves acute biochemical disruption, often detectable within minutes. The intermediate phase features cellular injury, inflammation, and functional impairment observable in blood chemistry and histopathology. The terminal phase culminates in organ failure or death if compensatory mechanisms are exhausted.
Experimental assessment of toxicity in mice relies on standardized protocols: LD₅₀ determination, observation of behavioral changes, measurement of body temperature, and post‑mortem organ analysis. Ethical guidelines require minimization of suffering, use of the smallest effective cohort, and implementation of humane endpoints.
Understanding these mechanisms enables accurate risk evaluation, selection of appropriate antidotes, and development of therapeutic interventions tailored to the specific toxic pathway involved.