Fenpropathrin exposure induces neurotoxicity in zebrafish embryos

Area of Science:

• Environmental Toxicology
• Developmental Neurobiology
• Ecotoxicology

Background:

• Fenpropathrin is a widely used insecticide with environmental and aquatic organism risks.
• Its impact on aquatic life, particularly nervous system development, is poorly understood.

Purpose of the Study:

• To evaluate the neurodevelopmental toxicity of fenpropathrin using zebrafish embryos.
• To investigate the mechanisms underlying fenpropathrin-induced neurotoxicity.

Main Methods:

• Zebrafish embryos were exposed to varying doses of fenpropathrin (0.016–0.064 mg/L) from 6 to 96 hours post-fertilization.
• Assessed physiological, behavioral, and neurodevelopmental endpoints.
• Analyzed gene expression related to neurodevelopment, neurotransmission, oxidative stress, and apoptosis.

Main Results:

• Fenpropathrin exposure caused enhanced acetylcholinesterase activity, abnormal swimming, brain cell abnormalities, and disrupted neuron migration.
• Neurodevelopmental and neurotransmitter gene expression was inhibited.
• Oxidative stress was induced, evidenced by increased reactive oxygen species (ROS) and reduced antioxidant enzymes (catalase, superoxide dismutase).
• Apoptosis was observed in brain and heart cells, with altered expression of apoptosis-associated and Nrf2 signaling pathway genes.

Conclusions:

• Fenpropathrin induces significant neurodevelopmental and behavioral impairments in zebrafish embryos.
• Oxidative stress and apoptosis are key mechanisms in fenpropathrin-induced neurotoxicity.
• The findings underscore the potential ecological risks of fenpropathrin to aquatic organisms.