PUBLICATION

Trimethyltin chloride induces reactive oxygen species-mediated apoptosis in retinal cells during zebrafish eye development

Authors
Kim, J., Kim, C.Y., Oh, H., Ryu, B., Kim, U., Lee, J.M., Jung, C.R., Park, J.H.
ID
ZDB-PUB-181107-18
Date
2018
Source
The Science of the total environment   653: 36-44 (Journal)
Registered Authors
Park, Jae-Hak
Keywords
Apoptosis, Ocular developmental toxicity, Reactive oxygen species, Trimethyltin chloride, Zebrafish
MeSH Terms
  • Animals
  • Apoptosis/drug effects*
  • Embryonic Development/drug effects*
  • Eye/drug effects*
  • Eye/embryology
  • Eye/growth & development
  • Gene Expression Profiling
  • Reactive Oxygen Species/metabolism*
  • Trimethyltin Compounds/adverse effects*
  • Water Pollutants, Chemical/adverse effects*
  • Zebrafish/embryology*
PubMed
30399559 Full text @ Sci. Total Environ.
Abstract
Trimethyltin chloride (TMT), one of the most widely used organotin compounds in industrial and agricultural fields, is widespread in soil, aquatic systems, foodstuffs and household items. TMT reportedly has toxic effects on the nervous system; however, there is limited information about its effects on eye development and no clear associated mechanisms have been identified. Therefore, in the present study, we investigated eye morphology, vison-related behavior, reactive oxygen species (ROS) production, apoptosis, histopathology, and gene expression to evaluate the toxicity of TMT during ocular development in zebrafish embryos. Exposure to TMT decreased the axial length and surface area of the eye and impaired the ability of zebrafish to recognize light. 2',7'-dichlorofluorescein diacetate and acridine orange assays revealed dose-dependent increases in ROS formation and apoptosis in the eye. Furthermore, pyknosis of retinal cells was confirmed through histopathological analysis. Antioxidative enzyme-related genes were downregulated and apoptosis-inducing genes were upregulated in TMT-treated zebrafish compared to expression in controls. Retinal cell-specific gene expression was suppressed mainly in retinal ganglion cells, bipolar cells, and photoreceptor cells, whereas amacrine cell-, horizontal cell-, and Müller cell-specific gene expression was enhanced. Our results demonstrate for the first time the toxicity of TMT during eye development, which occurs through the induction of ROS-mediated apoptosis in retinal cells during ocular formation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping