Ethanol exposure alters zebrafish development: A novel model of fetal alcohol syndrome

Bilotta, Joseph; Barnett, Jalynn A.; Hancock, Laura; Saszik, Shannon

doi:10.1016/j.ntt.2004.06.011

Cited by 169 publications

(150 citation statements)

References 14 publications

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“…Recently three laboratories independently documented measurable ethanol-induced phenotypic features in zebrafish that could be utilized further for analysis of ethanol-responsive genes (Bilotta et al, 2004;Carvan et al, 2004;Loucks and Carvan, 2004;Reimers et al, 2004a). As shown here and in previous studies, the Japanese medaka is an alternative non-mammalian model, in addition to zebrafish, to evaluate ethanol toxicity.…”

Section: Discussionmentioning

confidence: 62%

“…Large-scale mutagenic screens in zebrafish and medaka have identified several orthologue genes that are related closely to those involved in human genetic diseases (Naruse et al, 2004). The response of zebrafish embryos to ethanol has been studied by many investigators and zebrafish have been recognized as a useful model for the study of alcohol-induced teratogenic effects (Bilotta et al, 2004;Carvan et al, 2004;Lockwood et al, 2004;Reimers et al, 2004a). In zebrafish, ethanol causes cyclopia, affects visual functions, induces pericardial edema and otolith defects, lowers heart rate, reduces eye diameter, induces axial malformations, delays development, and produces axial blistering (Bilotta et al, 2002(Bilotta et al, , 2004Reimers et al, 2004a).…”

Section: Introductionmentioning

confidence: 99%

“…The response of zebrafish embryos to ethanol has been studied by many investigators and zebrafish have been recognized as a useful model for the study of alcohol-induced teratogenic effects (Bilotta et al, 2004;Carvan et al, 2004;Lockwood et al, 2004;Reimers et al, 2004a). In zebrafish, ethanol causes cyclopia, affects visual functions, induces pericardial edema and otolith defects, lowers heart rate, reduces eye diameter, induces axial malformations, delays development, and produces axial blistering (Bilotta et al, 2002(Bilotta et al, , 2004Reimers et al, 2004a). In addition, ethanol exposure has been shown to alter gene expression in the ventral aspects of the fore-and mid-brain (Blader and Strahle, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Wang

Williams

Haasch

et al. 2006

Birth Defects Research Pt B

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BACKGROUND: Animal models are necessary to investigate the mechanism of alcohol-induced birth defects. We have used Japanese medaka (Oryzias latipes) as a non-mammalian model to elucidate the molecular mechanism(s) of ethanol teratogenesis. METHODS: Medaka eggs, within 1 hr post-fertilization (hpf) were exposed to waterborne ethanol (0-1000 mM) in hatching solution for 48 hr. Embryo development was observed daily until 10 days post-fertilization (dpf). The concentration of embryonic ethanol was determined enzymatically. Cartilage and bones were stained by Alcian blue and calcein, respectively and skeletal and cardiovascular defects were assessed microscopically. Genetic gender of the embryos was determined by PCR. Levels of two isoenzymes of alcohol dehydrogenase (Adh) mRNAs were determined by semi-quantitative and real-time RT-PCR. RESULTS: The concentration of ethanol required to cause 50% mortality (LC 50 ) in 10 dpf embryos was 568 mM, however, the embryo absorbed only 15-20% of the waterborne ethanol at all ethanol concentrations. The length of the lower jaw and calcification in tail fin cartilaginous structures were reduced by ethanol exposure. Active blood circulation was exhibited at 501 hpf in embryos treated with 0-100 mM ethanol; active circulation was delayed and blood clots developed in embryos treated with 200-400 mM ethanol. The deleterious effects of ethanol were not gender-specific. Moreover, ethanol treatment was unable to alter the constitutive expression of either Adh5 or Adh8 mRNA in the medaka embryo. CONCLUSIONS: Preliminary results suggested that embryogenesis in medaka was significantly affected by ethanol exposure. Phenotypic features normally associated with ethanol exposure were similar to that observed in mammalian models of fetal alcohol syndrome. The results further indicated that medaka embryogenesis might be used as an alternative non-mammalian model for investigating specific alterations in gene expression as a means to understand the molecular mechanism(s) of ethanol-induced birth defects.

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Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Wang

Williams

Haasch

et al. 2006

Birth Defects Research Pt B

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“…[55][56][57][58][59] We have extended these results by using this model to identify a novel molecular mechanism that may be responsible for alcohol's teratogenic effects, namely, alcoholinduced inhibition of the cholesterol modification of Shh, which subsequently inhibits Shh signal transduction; inhibition of this pathway appears to play the key role in the development of FASD pathogenesis. As zebrafish lack placentas and develop ex utero, and alcohol dehydrogenases 60,61 are not expressed in embryos at the time exposed to alcohol (ie from 4-10 hpf), Thus, the metabolites generated by oxidation of ethanol are not likely to be a major cause of the induced phenotypes.…”

Section: Discussionmentioning

confidence: 97%

Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Yang

Zdanowicz

et al. 2007

Laboratory Investigation

135

144

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“…43,44 A separate study suggested that the eye diameter was sensitive to even 0.4% ethanol. 45 The difference between these findings is unclear, but may relate to genetic background as Dlugos and Rabin 45 used an outbred background and Bilotta et al 43,44 used an unspecified background. The earliest use of zebrafish in FASD research focused on structural defects caused by ethanol.…”

Section: Zebrafish Models Of Fasdmentioning

confidence: 99%

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

2016

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Fetal Alcohol Spectrum Disorders (FASD) describes a wide array of ethanol-induced developmental defects, including craniofacial dysmorphology and cognitive impairments. It affects *1 in 100 children born in the United States each year. Due to the pleiotropic effects of ethanol, animal models have proven critical in characterizing the mechanisms of ethanol teratogenesis. In this review, we focus on the utility of zebrafish in characterizing ethanolinduced developmental defects. A growing number of laboratories have focused on using zebrafish to examine ethanol-induced defects in craniofacial, cardiac, ocular, and neural development, as well as cognitive and behavioral impairments. Growing evidence supports that genetic predisposition plays a role in these ethanol-induced defects, yet little is understood about these gene-ethanol interactions. With a high degree of genetic amenability, zebrafish is at the forefront of identifying and characterizing the gene-ethanol interactions that underlie FASD.

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Ethanol exposure alters zebrafish development: A novel model of fetal alcohol syndrome

Cited by 169 publications

References 14 publications

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

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