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Article: Cadmium affects retinogenesis during zebrafish embryonic development

TitleCadmium affects retinogenesis during zebrafish embryonic development
Authors
Issue Date2009
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology and Applied Pharmacology, 2009, v. 235 n. 1, p. 68-76 How to Cite?
AbstractOcular malformations are commonly observed in embryos of aquatic species after exposure to toxicants. Using zebrafish embryos as the model organism, we showed that cadmium exposure from sphere stage (4 hpf) to end of segmentation stage (24 hpf) induced microphthalmia in cadmium-treated embryos. Embryos with eye defects were then assessed for visual abilities. Cadmium-exposed embryos were behaviorally blind, showing hyperpigmentation and loss of camouflage response to light. We investigated the cellular basis of the formation of the small eyes phenotype and the induction of blindness by studying retina development and retinotectal projections. Retinal progenitors were found in cadmium-treated embryos albeit in smaller numbers. The number of retinal ganglion cells (RGC), the first class of retinal cells to differentiate during retinogenesis, was reduced, while photoreceptor cells, the last batch of retinal neurons to differentiate, were absent. Cadmium also affected the propagation of neurons in neurogenic waves. The neurons remained in the ventronasal area and failed to spread across the retina. Drastically reduced RGC axons and disrupted optic stalk showed that the optic nerves did not extend from the retina beyond the chiasm into the tectum. Our data suggested that impairment in neuronal differentiation of the retina, disruption in RGC axon formation and absence of cone photoreceptors were the causes of microphthalmia and visual impairment in cadmium-treated embryos.
Persistent Identifierhttp://hdl.handle.net/10722/129017
ISSN
2015 Impact Factor: 3.847
2015 SCImago Journal Rankings: 1.593
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, ChinaCityU 1474/05M
Funding Information:

The work described in this paper was fully supported by a grant from the Research Grants Council of the Hong Kong Special Administrative Region, China (Project No. CityU 1474/05M). The authors declare that there are no conflicts of interest.

 

DC FieldValueLanguage
dc.contributor.authorChow, ESH-
dc.contributor.authorHui, MNY-
dc.contributor.authorCheng, CW-
dc.contributor.authorCheng, SH-
dc.date.accessioned2010-12-17T04:06:13Z-
dc.date.available2010-12-17T04:06:13Z-
dc.date.issued2009-
dc.identifier.citationToxicology and Applied Pharmacology, 2009, v. 235 n. 1, p. 68-76-
dc.identifier.issn0041-008X-
dc.identifier.urihttp://hdl.handle.net/10722/129017-
dc.description.abstractOcular malformations are commonly observed in embryos of aquatic species after exposure to toxicants. Using zebrafish embryos as the model organism, we showed that cadmium exposure from sphere stage (4 hpf) to end of segmentation stage (24 hpf) induced microphthalmia in cadmium-treated embryos. Embryos with eye defects were then assessed for visual abilities. Cadmium-exposed embryos were behaviorally blind, showing hyperpigmentation and loss of camouflage response to light. We investigated the cellular basis of the formation of the small eyes phenotype and the induction of blindness by studying retina development and retinotectal projections. Retinal progenitors were found in cadmium-treated embryos albeit in smaller numbers. The number of retinal ganglion cells (RGC), the first class of retinal cells to differentiate during retinogenesis, was reduced, while photoreceptor cells, the last batch of retinal neurons to differentiate, were absent. Cadmium also affected the propagation of neurons in neurogenic waves. The neurons remained in the ventronasal area and failed to spread across the retina. Drastically reduced RGC axons and disrupted optic stalk showed that the optic nerves did not extend from the retina beyond the chiasm into the tectum. Our data suggested that impairment in neuronal differentiation of the retina, disruption in RGC axon formation and absence of cone photoreceptors were the causes of microphthalmia and visual impairment in cadmium-treated embryos.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap-
dc.relation.ispartofToxicology and Applied Pharmacology-
dc.subject.meshAnimals-
dc.subject.meshCadmium - toxicity-
dc.subject.meshEmbryo, Nonmammalian - drug effects-
dc.subject.meshRetina - cytology - drug effects - embryology-
dc.subject.meshZebrafish - embryology-
dc.titleCadmium affects retinogenesis during zebrafish embryonic developmenten_US
dc.typeArticleen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0041-008X&volume=235&issue=1&spage=68&epage=76&date=2009&atitle=Cadmium+affects+retinogenesis+during+zebrafish+embryonic+development-
dc.identifier.emailCheng, CW: primerdimer@yahoo.com-
dc.identifier.emailCheng, SH: bhcheng@cityu.edu.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.taap.2008.11.013-
dc.identifier.pmid19100278-
dc.identifier.scopuseid_2-s2.0-59149083063-
dc.identifier.hkuros166379-
dc.identifier.volume235-
dc.identifier.issue1-
dc.identifier.spage68-
dc.identifier.epage76-
dc.identifier.isiWOS:000263541600009-

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