PUBLICATION
Mechanisms of cadmium-caused eye hypoplasia and hypopigmentation in zebrafish embryos
- Authors
- Zhang, T., Zhou, X.Y., Ma, X.F., Liu, J.X.
- ID
- ZDB-PUB-150816-2
- Date
- 2015
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 167: 68-76 (Journal)
- Registered Authors
- Liu, Jing-xia, Zhang, Ting
- Keywords
- BIO, Cadmium, High-throughput in situ hybridization screening, Neural crest, Pigment cells, RA, Zebrafish
- MeSH Terms
-
- Animals
- Cadmium/toxicity*
- Embryo, Nonmammalian/drug effects*
- Embryonic Development/drug effects
- Hypopigmentation/chemically induced
- Neural Crest/drug effects
- Water Pollutants, Chemical/toxicity*
- Zebrafish/embryology*
- PubMed
- 26276355 Full text @ Aquat. Toxicol.
Citation
Zhang, T., Zhou, X.Y., Ma, X.F., Liu, J.X. (2015) Mechanisms of cadmium-caused eye hypoplasia and hypopigmentation in zebrafish embryos. Aquatic toxicology (Amsterdam, Netherlands). 167:68-76.
Abstract
Cadmium-caused head and eye hypoplasia and hypopigmentation has been recognized for a long time, but knowledge of the underlying mechanisms is limited. In this study, we found that high mortality occurred in exposed embryos after 24hpf, when cadmium (Cd) dosage was above 17.8μM. Using high-throughput in situ hybridization screening, we found that genes labelling the neural crest and its derivative pigment cells exhibited obviously reduced expression in Cd-exposed embryos from 24hpf, 2 days earlier than head and eye hypoplasia and hypopigmentation occurred. Moreover, based on expression of crestin, a neural crest marker, we found that embryos before the gastrula stage were more sensitive to cadmium toxicity and that damage caused by Cd on embryogenesis was dosage dependent. In addition, by phenotype observation and detection of neural crest and pigment cell markers, we found that BIO and retinoic acid (RA) could neutralize the toxic effects of Cd on zebrafish embryogenesis. In this study, we first determined that Cd blocked the formation of the neural crest and inhibited specification of pigment cells, which might contribute to the molecular mechanisms underlying the phenotype defects of head and eye hypoplasia and hypopigmentation in Cd-exposed embryos. Moreover, we found that compounds BIO or RA could neutralize the toxic effects of Cd.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping