Supraphysiological acetaldehyde levels suppress growth in chicken embryos

Hartl, Michael; Shibley, Ivan A.

doi:10.1016/s0741-8329(02)00272-0

Cited by 4 publications

(2 citation statements)

References 41 publications

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“…On the other hand, direct administration of acetaldehyde is teratogenic in both mouse and zebrafish (Reimers et al, 2004; Webster et al, 1983), suggesting there may be some role for this metabolite in FASD. However, across several strains of chickens levels of acetaldehyde had to be beyond physiological levels to cause embryo malformations (Hartl and Shibley, 2002). Ethanol-exposure alters the activity of Adh and Aldh enzymes in rat (Boleda et al, 1992; Messiha and Varma, 1983), further complicating which metabolic enzymes are most relevant to FASD.…”

Section: Fasd Geneticsmentioning

confidence: 99%

The Genetics of Fetal Alcohol Spectrum Disorders

Eberhart¹,

Parnell

2016

Alcoholism Clin & Exp Res

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Background The term Fetal Alcohol Spectrum Disorders (FASD) defines the full range of ethanol-induced birth defects. Numerous variables influence the phenotypic outcomes of embryonic ethanol exposure. Among these variables, genetics appears to play an important role yet our understanding of the genetic predisposition to FASD is still in its infancy. Methods We review the current literature that relates to the genetics of FASD susceptibility and gene-ethanol interactions. Where possible, we comment on potential mechanisms of reported gene-ethanol interactions. Results Early indications of genetic sensitivity to FASD came from human and animal studies using twins or inbred strains, respectively. These analyses prompted searches for susceptibility loci involved in ethanol metabolism and analyses of candidate loci, based on phenotypes observed in FASD. More recently, genetic screens in animal models have provided additional insight into the genetics of FASD Conclusions Understanding FASD requires that we understand the many factors influencing phenotypic outcome following embryonic ethanol exposure. We are gaining ground on understanding some of the genetics behind FASD, yet much work remains to be done. Coordinated analyses using human patients and animal models are likely to be highly fruitful in uncovering the genetics behind FASD.

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Section: Fasd Geneticsmentioning

confidence: 99%

The Genetics of Fetal Alcohol Spectrum Disorders

Eberhart¹,

Parnell

2016

Alcoholism Clin & Exp Res

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“…Bupp-Becker and Shibley (1998) similarly found genetic influences upon alcohol-mediated growth suppression (42 – 78 mg/egg), and two broiler strains (Peterson x Hubbard; Ross x HY) had greater growth reductions in response to graded alcohol exposures compared with two layer strains (DeKalb Gold, White Leghorn unspecified); this may reflect that broilers are under intense genetic selection for rapid growth and muscle accumulation, whereas layer strain selection emphasizes early sex dimorphism and egg production. These two broiler strains also showed greater growth reductions in response to acetaldehyde than did layer W36 Ginther White Leghorn (Hartl and Shibley 2002). DeKalb Gold had greater resistance to alcohol lethality than the other strains (Bupp-Becker and Shibley 1998), work that was later mirrored in our group (50 mM for 2-3hr, 20 mg/egg) as DeKalb strains were less vulnerable to heart defects (Cavieres and Smith, 1999), neural crest death (Debelak and Smith 2000), and facial anomalies (Su et al 2001).…”

Section: Mechanistic Insights From Avian Models Of Fasdmentioning

confidence: 89%

The avian embryo as a model for fetal alcohol spectrum disorder

Flentke

Smith

2018

Biochem. Cell Biol.

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Prenatal alcohol exposure (PAE) remains a leading preventable cause of structural birth defects and permanent neurodevelopmental disability. The chick (Gallus gallus domesticus) is a powerful embryological research model and was possibly the first (Fere, 1895) in which alcohol’s teratogenicity was demonstrated. Pharmacologically relevant alcohol exposures in the range of 20–70 mM (20–80 mg/egg) disrupt chick embryo growth, morphogenesis, and behavior, and the resulting phenotypes strongly parallel those of mammalian models. The avian embryo’s direct accessibility has enabled novel insights into alcohol’s teratogenic mechanisms. These include the contribution of IGF1 signaling to growth suppression, the altered flow dynamics that reshape valvuloseptal morphogenesis and mediate its cardiac teratogenicity, and the suppression of Wnt and Shh signals to disrupt neural crest migration, expansion, and survival and underlie its characteristic craniofacial deficits. The genetic diversity within commercial avian strains enabled identification of unique loci, such as ribosome biogenesis, that modify vulnerability to alcohol. This venerable research model is equally relevant for the future, as the application of technological advances including CRISPR, optogenetics, and biophotonics to the embryo’s ready accessibility creates a unique model in which investigators can manipulate and monitor the embryo in real-time to investigate alcohol’s actions upon cell fate.

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