How does dichlorvos affect rats? - briefly
Dichlorvos, an organophosphate insecticide, inhibits acetylcholinesterase in rats, causing acetylcholine accumulation and cholinergic overstimulation. Clinical manifestations include tremors, excessive salivation, respiratory distress, and rapid mortality at lethal concentrations.
How does dichlorvos affect rats? - in detail
Dichlorvos, an organophosphate insecticide, inhibits acetylcholinesterase (AChE) activity in rat nervous tissue. The inhibition leads to accumulation of acetylcholine at synaptic junctions, causing continuous stimulation of muscarinic and nicotinic receptors.
Acute exposure at doses near the oral LD₅₀ (≈ 12 mg kg⁻¹) produces rapid onset of cholinergic crisis. Clinical signs include salivation, lacrimation, bronchorrhea, tremors, convulsions, and respiratory failure. Mortality typically occurs within minutes to hours, depending on dose and route of administration.
Sublethal concentrations generate measurable biochemical and physiological alterations:
- AChE activity reduced by 30–80 % in brain, liver, and blood within 24 h.
- Elevated serum cholinesterase correlates with impaired motor coordination on rotarod tests.
- Decreased heart rate and blood pressure due to excessive parasympathetic stimulation.
- Hepatocellular vacuolation and centrilobular necrosis observed in histopathology.
- Renal tubular degeneration evident after repeated dosing.
Behavioral effects manifest as reduced exploratory activity, increased anxiety‑like responses in elevated plus‑maze assays, and impaired learning in passive avoidance tasks. Chronic exposure, even at low ppm levels in feed, leads to persistent neurochemical deficits and delayed growth, reflected in lower body weight gain and reduced organ weights.
Metabolic detoxification proceeds primarily through hepatic cytochrome P450 enzymes, converting dichlorvos to 2,2-dichlorovinyl dimethyl phosphate, which is excreted in urine. Species‑specific variations in enzyme expression influence susceptibility; rats display higher sensitivity compared with larger mammals.
Dose‑response relationships demonstrate a steep increase in mortality between 5 and 15 mg kg⁻¹, while sublethal endpoints show a linear decline in AChE activity with rising dose. These data support the classification of dichlorvos as a highly toxic agent for rodent models and underscore the need for stringent exposure limits in laboratory and pest‑control settings.