How does poison affect a rat? - briefly
Poison delivers toxic chemicals that impair cellular function, causing organ failure and death. Onset of symptoms varies from minutes to hours based on toxin potency and exposure route.
How does poison affect a rat? - in detail
Poison introduced into a rat’s system initiates a cascade of physiological disruptions that culminate in organ failure and death. The route of exposure—oral ingestion, intraperitoneal injection, inhalation, or dermal contact—determines the speed and pattern of absorption. Oral intake passes through the gastrointestinal tract, where the toxin is absorbed into the portal circulation and transported to the liver for metabolic processing. Intraperitoneal injection delivers the substance directly into the peritoneal cavity, allowing rapid entry into systemic circulation. Inhalation introduces volatile agents into the pulmonary alveoli, while dermal exposure relies on skin permeability and may be slower unless the compound is lipophilic.
Once in the bloodstream, the toxin interacts with specific cellular targets, often enzymes or ion channels, producing immediate biochemical alterations. Common mechanisms include:
- Enzyme inhibition – organophosphates bind acetylcholinesterase, causing accumulation of acetylcholine and uncontrolled neuronal firing.
- Ion channel blockade – cardiac glycosides obstruct Na⁺/K⁺‑ATPase, leading to arrhythmias and loss of contractile function.
- Oxidative stress – heavy metals generate free radicals, damaging membranes, proteins, and DNA.
- Metabolic disruption – cyanide interferes with cytochrome c oxidase, halting cellular respiration and inducing hypoxia.
These primary actions trigger secondary systemic effects. Neurological manifestations appear first: tremors, seizures, loss of coordination, and respiratory paralysis. Cardiovascular signs follow, including tachycardia, hypotension, and arrhythmias. Hepatic and renal tissues suffer from toxin‑induced necrosis, reflected in elevated enzyme levels and reduced filtration capacity. Coagulation pathways may become impaired, leading to hemorrhage or thrombosis depending on the agent.
The animal’s physiological response progresses through three phases:
- Acute phase (minutes to hours) – rapid onset of symptoms, marked by nervous‑system hyperactivity or depression, and circulatory collapse.
- Compensatory phase (hours to days) – activation of detoxifying enzymes, such as glutathione‑S‑transferase, attempts to neutralize the poison; however, organ damage may already be irreversible.
- Terminal phase (hours to days) – failure of critical organs, culminating in death if supportive care is absent.
Intervention strategies target each stage. Immediate decontamination (e.g., gastric lavage, activated charcoal) reduces absorption. Antidotes—such as atropine for cholinergic poisoning or hydroxocobalamin for cyanide—counteract specific molecular interactions. Supportive measures, including mechanical ventilation, fluid resuscitation, and electrolyte correction, sustain vital functions while the body metabolizes or excretes the toxin.
In experimental settings, dose‑response curves quantify lethality (LD₅₀ values) and inform safety thresholds. Variability arises from strain differences, age, sex, and prior exposure to other chemicals, underscoring the need for precise dosing and thorough monitoring.