Alcohol dehydrogenase activity in the developing chick embryo

Wilson, Robert; Kalmus, Gerhard W.; Pennington, Sam N.

doi:10.1016/0305-0491(84)90242-6

Cited by 24 publications

(6 citation statements)

References 18 publications

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“…These results are similar to those we reportcd previously (Swanson et al, 1994) and reflect the fact that, during the stages viewed, hepatic ethanol metabolism is just beginning, and the embryo is not yet able to clear ethanol efficiently (alcohol dehydrogenase activity is not detectable in the embryonic chick until E8; Wilson et al, 1984). It should be noted that these blood ethanol levels represent concentrations approximating those seen following acute or chronic ethanol consumption in both humans and in animal models and are also consistent with concentrations reaching the mammalian fetus under these conditions (Urso et al, 198 1;Church et al, 1990;Middaugh and Boggan, 1990).…”

Section: Embryonic Motilitysupporting

confidence: 92%

Ethanol influences on the chick embryo spinal cord motor system: Analyses of motoneuron cell death, motility, and target trophic factor activity and in vitro analyses of neurotoxicity and trophic factor neuroprotection

Heaton

Bradley

1995

J. Neurobiol.

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A series of in vivo and in vitro experiments were conducted to determine the influence of prenatally administered ethanol on several aspects of the developing chick embryo spinal cord motor system. Specifically, we examined: (1) the effect of chronic ethanol administration during the natural cell death period on spinal cord motoneuron numbers; (2) the influence of ethanol on ongoing embryonic motility; (3) the effect of ethanol exposure on neurotrophic activity in motoneuron target tissue (limb bud); and (4) the responsiveness of cultured spinal cord neurons to ethanol, and the potential of target-derived neurotrophic factors to ameliorate ethanol neurotoxicity. These studies revealed the following: Chronic prenatal ethanol exposure reduces the number of motoneurons present in the lateral motor column after the cell death period [embryonic day 12 (E12)]. Ethanol tends to inhibit embryonic motility, particularly during the later stages viewed (E9-E11). Chronic ethanol exposure reduces the neurotrophic activity contained in target muscle tissue. Such diminished support could contribute to the observed motoneuron loss. Direct exposure of spinal cord neurons to ethanol decreases neuronal survival and process outgrowth in a dose-dependent manner, but the addition of target muscle extract to ethanol-containing cultures can ameliorate this ethanol neurotoxicity. These studies demonstrate ethanol toxicity in a population not previously viewed in this regard and suggest a mechanism that may be related to this cell loss (i.e., decreased neurotrophic support).

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Section: Embryonic Motilitysupporting

confidence: 92%

Ethanol influences on the chick embryo spinal cord motor system: Analyses of motoneuron cell death, motility, and target trophic factor activity and in vitro analyses of neurotoxicity and trophic factor neuroprotection

Heaton

Bradley

1995

J. Neurobiol.

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“…Another source of discussion is whether ethanol itself or its principal metabolite, acetaldehyde, is responsible for the NCC changes involved in FAS. Data from early avian experimental models support the first point of view (Cartwright and Smith, 1995, and this study), inasmuch as the enzymatic capacity of class I alcohol dehydrogenase to metabolize ethanol is reached only after 9 days of chick embryo development (Wilson et al, 1984), and there is no direct evidence of the production of acetaldehyde by in vitro neural cells (Eysseric et al, 1997). However, data from transgenic mice examining the gene encoding class IV alcohol dehydrogenase-although weakly effective as an ethanol dehydrogenase-suggest its potential participation in the mechanism of alcohol-induced craniofacial defects (Haselbeck and Duester, 1998).…”

Section: Discussionsupporting

confidence: 77%

Ethanol Induces Morphological and Dynamic Changes on In Vivo and In Vitro Neural Crest Cells

Rovasio

Battiato

2002

Alcoholism Clin & Exp Res

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Taking into account that even a limited period of abnormal behavior may imply serious consequences in the final cues of an embryonic cell population, our results indicate that the biological effects of ethanol on early development-even during a short time-could induce permanent ontogenetic perturbations of NCCs, with potentially dramatic effects on embryonic morphogenesis. These results support an important participation of NCCs in the etiopathogeny of FAS.

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“…Direct application of alcohol to the embryo within a windowed egg should never be used due to osmotic effects that cause non-specific damage. Chick embryos have little-to-no alcohol metabolism until day nine of incubation (Wilson et al 1984). Chick liver ADH has a Km of 0.10 to 0.52 mmol and Vmax of 1.15 ± 0.3 μmol/min/g (Sinclair et al 1990).…”

Section: Experimental Factors For Avian Models Of Developmental Alcohmentioning

confidence: 99%

“…Studies using the ADH inhibitor pyrazole affirmed ethanol as the proximate teratogen (Gilani et al 1986). The egg shell is weakly porous to alcohol and losses average ~5% daily until day 11, when liver metabolism rapidly clears the remainder (Wilson et al 1984). Thus, chick typically represents a chronic binge model.…”

Section: Experimental Factors For Avian Models Of Developmental Alcohmentioning

confidence: 99%

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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Alcohol dehydrogenase activity in the developing chick embryo

Cited by 24 publications

References 18 publications

Ethanol influences on the chick embryo spinal cord motor system: Analyses of motoneuron cell death, motility, and target trophic factor activity and in vitro analyses of neurotoxicity and trophic factor neuroprotection

Ethanol influences on the chick embryo spinal cord motor system: Analyses of motoneuron cell death, motility, and target trophic factor activity and in vitro analyses of neurotoxicity and trophic factor neuroprotection

Ethanol Induces Morphological and Dynamic Changes on In Vivo and In Vitro Neural Crest Cells

The avian embryo as a model for fetal alcohol spectrum disorder

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