PUBLICATION

Fenpropathrin causes alterations in locomotion and social behaviors in zebrafish (Danio rerio)

Authors
Liu, S.T., Horng, J.L., Lin, L.Y., Chou, M.Y.
ID
ZDB-PUB-231114-3
Date
2023
Source
Aquatic toxicology (Amsterdam, Netherlands)   265: 106756106756 (Journal)
Registered Authors
Chou, Ming-Yi, Horng, Jiun-Lin
Keywords
Dopaminergic neurons, Fenpropathrin, Locomotion, Zebrafish
MeSH Terms
  • Animals
  • Behavior, Animal
  • Locomotion
  • Mammals
  • Pyrethrins*/toxicity
  • Social Behavior
  • Water Pollutants, Chemical*/toxicity
  • Zebrafish/metabolism
PubMed
37952273 Full text @ Aquat. Toxicol.
Abstract
Fenpropathrin is one of the widely used pyrethroid pesticides in agriculture and is frequently detected in the environment, groundwater, and food. While fenpropathrin was found to have neurotoxic effects in mammals, it remains unclear whether it has similar effects on fish. Here, we used adult zebrafish to investigate the impacts of fenpropathrin on fish social behaviors and neural activity. Exposure of adult zebrafish to 500 ppb of fenpropathrin for 72 h increased anxiety levels but decreased physical fitness, as measured by a novel tank diving test and swimming tunnel test. Fish exposed to fenpropathrin appeared to spend more time in the conspecific zone of the tank, possibly seeking greater comfort from their companions. Although learning, memory, and aggressive behavior did not change, fish exposed to fenpropathrin appeared to have shorter fighting durations. The immunocytochemical results showed the tyrosine hydroxylase antibody-labeled dopaminergic neurons in the teleost posterior tuberculum decreased in the zebrafish brain. According to a quantitative polymerase chain reaction (qPCR) analysis of the brain, exposure to fenpropathrin resulted in a decrease in the messenger (m)RNA expression of monoamine oxidase (mao), an enzyme that facilitates the deamination of dopamine. In contrast, the mRNA expression of the sncga gene, which may trigger Parkinson's disease, was found to have increased. There were no changes observed in expressions of genes related to antioxidants and apoptosis between the control and fenpropathrin-exposed groups. We provide evidence to demonstrate the defect of the neurotoxicity of fenpropathrin toward dopaminergic neurons in adult zebrafish.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping