PUBLICATION

Triclosan affects axon formation in the neural development stages of zebrafish embryos (Danio rerio)

Authors
Kim, J., Oh, H., Ryu, B., Kim, U., Lee, J.M., Jung, C.R., Kim, C.Y., Park, J.H.
ID
ZDB-PUB-180208-12
Date
2018
Source
Environmental pollution (Barking, Essex : 1987)   236: 304-312 (Journal)
Registered Authors
Lee, Ji-Min, Park, Jae-Hak
Keywords
Axonogenesis, Developmental neurotoxicity, Triclosan, Zebrafish
MeSH Terms
  • Luminescent Proteins/genetics
  • Animals
  • Embryo, Nonmammalian/abnormalities
  • Embryo, Nonmammalian/drug effects*
  • Triclosan/toxicity*
  • Animals, Genetically Modified/abnormalities
  • Animals, Genetically Modified/embryology
  • Animals, Genetically Modified/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Central Nervous System/abnormalities
  • Central Nervous System/drug effects*
  • Central Nervous System/embryology
  • Anti-Infective Agents, Local/toxicity*
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Neurogenesis/drug effects*
  • Axons/drug effects*
  • Gene Expression Regulation, Developmental/drug effects
(all 18)
PubMed
29414352 Full text @ Environ. Pollut.
Abstract
Triclosan (TCS) is an organic compound with a wide range of antibiotic activity and has been widely used in items ranging from hygiene products to cosmetics; however, recent studies suggest that it has several adverse effects. In particular, TCS can be passed to both fetus and infants, and while some evidence suggests in vitro neurotoxicity, there are currently few studies concerning the mechanisms of TCS-induced developmental neurotoxicity. Therefore, this study aimed to clarify the effect of TCS on neural development using zebrafish models, by analyzing the morphological changes, the alterations observed in fluorescence using HuC-GFP and Olig2-dsRED transgenic zebrafish models, and neurodevelopmental gene expression. TCS exposure decreased the body length, head size, and eye size in a concentration-dependent manner in zebrafish embryos. It increased apoptosis in the central nervous system (CNS) and particularly affected the structure of the CNS, resulting in decreased synaptic density and shortened axon length. In addition, it significantly up-regulated the expression of genes related to axon extension and synapse formation such as ?1-Tubulin and Gap43, while decreasing Gfap and Mbp related to axon guidance, myelination and maintenance. Collectively, these changes indicate that exposure to TCS during neurodevelopment, especially during axonogenesis, is toxic. This is the first study to demonstrate the toxicity of TCS during neurogenesis, and suggests a possible mechanism underlying the neurotoxic effects of TCS in developing vertebrates.
Genes / Markers
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Expression
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Phenotype
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Mutations / Transgenics
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Human Disease / Model
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Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
No data available
Mapping