ArticlePloS one2017
Ethanol itself is a holoprosencephaly-inducing teratogen.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Developmental Neurotoxicity of Alcohol from Neuronal Basis to Behavioural Outcomes: A Comprehensive Review.Neurology international · 2026Review
- Cyclopia: Facial deformity indicating severe holoprosencephaly with imaging findings of brain: A case report.Radiology case reports · 2026Article
- A register-based study of long-term health and social care costs among children with prenatal alcohol exposure.PloS one · 2026Article
- A Rare Case Report on Holoprosencephaly With Cyclopia: Jimma University Medical Center, Ethiopia.Case reports in obstetrics and gynecology · 2026Article
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- High-throughput detection of craniofacial defects in fluorescent zebrafish.Birth defects research · 2023Article
- Cyclopia in a newborn rhesus macaque born to a dam infected with SIV and receiving antiretroviral therapy during pregnancy.Current trends in immunology · 2023Article
- Gene-alcohol interactions in birth defects.Current topics in developmental biology · 2023Article
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Ethanol Effects on Early Developmental Stages Studied Using the Zebrafish.Biomedicines · 2022Review
- Brain Organization and Human Diseases.Cells · 2022Review
- Cyclopia, a newborn with a single eye, a rare but lethal congenital anomaly: A case report.International journal of surgery case reports · 2021Article
- Gene-teratogen interactions influence the penetrance of birth defects by altering Hedgehog signaling strength.Development (Cambridge, England) · 2021Article
- Exposure to ethanol leads to midfacial hypoplasia in a zebrafish model of FASD via indirect interactions with the Shh pathway.BMC biology · 2021Article
- Diabetes, Oxidative Stress, and DNA Damage Modulate Cranial Neural Crest Cell Development and the Phenotype Variability of Craniofacial Disorders.Frontiers in cell and developmental biology · 2021Review
- Multifactorial Genetic and Environmental Hedgehog Pathway Disruption Sensitizes Embryos to Alcohol-Induced Craniofacial Defects.Alcoholism, clinical and experimental research · 2020Article
- Ocular measurements in fetal alcohol spectrum disorders.American journal of medical genetics. Part A · 2020Article
- Corpus Callosum Agenesis: An Insight into the Etiology and Spectrum of Symptoms.Brain sciences · 2020Review
- Article
- Lobar holoprosencephaly with craniofacial defects in a Friesian calf: A case report.Veterinary medicine and science · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ethanol is a teratogen, inducing a variety of structural defects in developing humans and animals that are exposed in utero. Mechanisms of ethanol teratogenicity in specific defects are not well understood. Oxidative metabolism of ethanol by alcohol dehydrogenase or cytochrome P450 2E1 has been implicated in some of ethanol's teratogenic effects, either via production of acetaldehyde or competitive inhibition of retinoic acid synthesis. Generalized oxidative stress in response to ethanol may also play a role in its teratogenicity. Among the developmental defects that ethanol has been implicated in is holoprosencephaly, a failure to define the midline of the forebrain and midface that is associated with a deficiency in Sonic hedgehog pathway function. Etiologically, holoprosencephaly is thought to arise from a complex combination of genetic and environmental factors. We have developed a gene-environment interaction model of holoprosencephaly in mice, in which mutation of the Sonic hedgehog coreceptor, Cdon, synergizes with transient in utero exposure to ethanol. This system was used to address whether oxidative metabolism is required for ethanol's teratogenic activity in holoprosencephaly. We report here that t-butyl alcohol, which is neither a substrate nor an inhibitor of alcohol dehydrogenases or Cyp2E1, is a potent inducer of holoprosencephaly in Cdon mutant mice. Additionally, antioxidant treatment did not prevent ethanol- or t-butyl alcohol-induced HPE in these mice. These findings are consistent with the conclusion that ethanol itself, rather than a consequence of its metabolism, is a holoprosencephaly-inducing teratogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.