How does dichlorvos affect mice? - briefly
Dichlorvos inhibits acetylcholinesterase, causing acute neurotoxicity that appears as tremors, paralysis, and respiratory distress in mice. Lethal effects arise at doses near 5–10 mg/kg, while lower exposures reduce motor coordination and enzyme activity.
How does dichlorvos affect mice? - in detail
Dichlorvos, an organophosphate insecticide, inhibits acetylcholinesterase (AChE) in murine nervous tissue. The enzyme blockade leads to accumulation of acetylcholine at cholinergic synapses, causing continuous stimulation of muscarinic and nicotinic receptors.
Acute exposure produces a rapid onset of signs:
- Salivation, lacrimation, and nasal discharge
- Tremors and muscle fasciculations
- Hyperventilation followed by respiratory depression
- Seizure activity and loss of righting reflex
- Mortality within minutes to hours, depending on dose
Sub‑lethal concentrations generate measurable biochemical and physiological alterations. Enzyme assays reveal a dose‑dependent reduction in AChE activity in brain, heart, and diaphragm, typically ranging from 30 % to 90 % inhibition at 0.5–2 mg kg⁻¹. Corresponding increases in plasma cholinesterase confirm systemic exposure.
Behavioral assessments show:
- Decreased locomotor activity in open‑field tests
- Impaired coordination on rotarod apparatus
- Altered grooming and nesting behavior, indicating central nervous system disruption
Cardiovascular monitoring records bradycardia and hypotension during the cholinergic phase, followed by tachycardia as compensatory mechanisms engage. Respiratory measurements demonstrate reduced tidal volume and increased respiratory rate, reflecting bronchoconstriction and central respiratory drive depression.
Histopathological examination of major organs reveals:
- Neuronal degeneration in the hippocampus and cerebral cortex
- Focal necrosis in hepatic lobules
- Vacuolation of renal tubular epithelium
- Inflammatory infiltrates in lung parenchyma
Dose‑response curves derived from LD₅₀ studies in laboratory mice place the median lethal dose at approximately 0.5 mg kg⁻¹ (oral) and 0.2 mg kg⁻¹ (intraperitoneal). Repeated low‑dose exposure produces cumulative AChE inhibition, leading to progressive symptom intensification and delayed mortality.
Experimental protocols recommend:
- Use of age‑matched, weight‑standardized animals
- Pre‑exposure baseline measurements of AChE activity
- Continuous observation for at least 24 h post‑administration
- Application of atropine or oxime antidotes to differentiate cholinergic effects from nonspecific toxicity
Safety considerations emphasize containment of vapors, personal protective equipment for handlers, and adherence to institutional animal care guidelines to minimize suffering and ensure reproducibility of results.