PUBLICATION

Developmental mechanisms of arsenite toxicity in zebrafish (Danio rerio) embryos

Authors
Li, D., Lu, C., Wang, J., Hu, W., Cao, Z., Sun, D., Xia, H., and Ma, X.
ID
ZDB-PUB-090106-30
Date
2009
Source
Aquatic toxicology (Amsterdam, Netherlands)   91(3): 229-237 (Journal)
Registered Authors
Keywords
Arsenite, Developmental toxicity, Zebrafish, Embryo, DNA methylation
MeSH Terms
  • Animals
  • Apoptosis/drug effects
  • Arsenites/toxicity*
  • Cell Proliferation/drug effects
  • DNA Methylation/drug effects
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/drug effects
  • Embryonic Development/drug effects*
  • Heart/drug effects
  • Heart/embryology
  • Nervous System/drug effects
  • Nervous System/embryology
  • Sodium Compounds/toxicity*
  • Survival Analysis
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/embryology*
PubMed
19110324 Full text @ Aquat. Toxicol.
Abstract
Arsenic usually accumulates in soil, water and airborne particles, from which it is taken up by various organisms. Exposure to arsenic through food and drinking water is a major public health problem affecting some countries. At present there are limited laboratory data on the effects of arsenic exposure on early embryonic development and the mechanisms behind its toxicity. In this study, we used zebrafish as a model system to investigate the effects of arsenite on early development. Zebrafish embryos were exposed to a range of sodium arsenite concentrations (0-10.0mM) between 4 and 120h post-fertilization (hpf). Survival and early development of the embryos were not obviously influenced by arsenite concentrations below 0.5mM. However, embryos exposed to higher concentrations (0.5-10.0mM) displayed reduced survival and abnormal development including delayed hatching, retarded growth and changed morphology. Alterations in neural development included weak tactile responses to light (2.0-5.0mM, 30hpf), malformation of the spinal cord and disordered motor axon projections (2.0mM, 48hpf). Abnormal cardiac function was observed as bradycardia (0.5-2.0mM, 60hpf) and altered ventricular shape (2.0mM, 48hpf). Furthermore, altered cell proliferation (2.0mM, 24hpf) and apoptosis status (2.0mM, 24 and 48hpf), as well as abnormal genomic DNA methylation patterning (2.0mM, 24 and 48hpf) were detected in the arsenite-treated embryos. All of these indicate a possible relationship between arsenic exposure and developmental failure in early embryogenesis. Our studies suggest that the negative effects of arsenic on vertebrate embryogenesis are substantial.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping