Effect of subacute poisoning with bifenthrin on locomotor activity, memory retention, haematological, biochemical and

B Nieradko-Iwanicka1, A Borzecki, B Jodlowska-Jedrych

  • 1Chair and Department of Hygiene, Medical University of Lublin, Lublin, Poland. bnieradkoiwanicka@wp.pl.

Abstract

Insights

Subacute exposure to bifenthrin (BIF) insecticide impairs memory and motor activity in mice. This pyrethroid also causes liver damage and alters blood, potentially through oxidative stress.

Area of Science:

  • Toxicology
  • Neuroscience
  • Environmental Health

Background:

  • Pyrethroids (PYRs), including bifenthrin (BIF), target insect sodium channels but human/animal exposure is a concern.
  • Chronic low-level exposure to PYRs occurs through various environmental pathways.
  • Uncertainty exists regarding dose-additive effects, extra-neural target organs, and common mechanisms of BIF toxicity.

Purpose of the Study:

  • To investigate the effects of subacute BIF exposure on memory, motor activity, and physiological parameters in mice.
  • To explore potential target organs beyond the brain and common toxicological mechanisms of BIF.

Main Methods:

  • Mice received daily intraperitoneal injections of BIF (4 or 8 mg/kg) for 28 days.
  • Motor activity was assessed on days 1, 7, 14, and 28.
  • Memory retention was tested using a passive avoidance task, and hematological, biochemical, and histopathological analyses were performed.

Main Results:

  • BIF significantly impaired memory retention early in the study (day 2).
  • Locomotor activity was dose-dependently decreased throughout the 28-day period without cumulative behavioral effects.
  • Subacute BIF exposure led to anemia, elevated white blood cell count, increased ALT and SOD, decreased GPx activity, and liver lymphocyte infiltrates.

Conclusions:

  • Subacute bifenthrin poisoning reduces locomotor activity proportionally to the dose.
  • BIF induces liver damage and hematological alterations in mice.
  • Oxidative stress is proposed as a potential unifying mechanism for BIF's toxic effects.