ArticleAlcohol (Fayetteville, N.Y.)2015
Zebrafish retinal defects induced by ethanol exposure are rescued by retinoic acid and folic acid supplement.
Article in Alcohol (Fayetteville, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Folic acid prevention of neural tube defects requires retinoic acid produced by ALDH1L1.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- The interaction between paracetamol and ethanol during the early development of zebrafish.Frontiers in pharmacology · 2026Article
- The Fetal Alcohol Spectrum Disorders-An Overview of Experimental Models, Therapeutic Strategies, and Future Research Directions.Children (Basel, Switzerland) · 2024Review
- Protective effects of resveratrol on the ethanol-induced disruption of retinogenesis in pluripotent stem cell-derived organoids.FEBS open bio · 2023Article
- Zebrafish as a Model to Study Retinoic Acid Signaling in Development and Disease.Biomedicines · 2023Review
- Alcohol induces neural tube defects by reducing retinoic acid signaling and promoting neural plate expansion.Frontiers in cell and developmental biology · 2023Article
- Microbiota and nutrition as risk and resiliency factors following prenatal alcohol exposure.Frontiers in neuroscience · 2023Review
- Ethanol Effects on Early Developmental Stages Studied Using the Zebrafish.Biomedicines · 2022Review
- Zebrafish Model of Stickler Syndrome Suggests a Role for Col2a1a in the Neural Crest during Early Eye Development.Journal of developmental biology · 2022Article
- Pharmacological activation of the Sonic hedgehog pathway with a Smoothened small molecule agonist ameliorates the severity of alcohol-induced morphological and behavioral birth defects in a zebrafish model of fetal alcohol spectrum disorder.Journal of neuroscience research · 2022Article
- Effects of nutrition and gestational alcohol consumption on fetal growth and development.Nutrition reviews · 2022Review
- Potential Biomarkers and Drugs for Nanoparticle-Induced Cytotoxicity in the Retina: Based on Regulation of Inflammatory and Apoptotic Genes.International journal of environmental research and public health · 2022Article
- Developmental, Behavioral and Transcriptomic Changes in Zebrafish Embryos after Smoke Dye Exposure.Toxics · 2022Article
- Developmental toxicity and neurotoxicity assessment of R-, S-, and RS-propylene glycol enantiomers in zebrafish (Danio rerio) larvae.Environmental science and pollution research international · 2022Article
- Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.PloS one · 2022Article
- Epigenetics and Neuroinflammation Associated With Neurodevelopmental Disorders: A Microglial Perspective.Frontiers in cell and developmental biology · 2022Review
- Reduced Retinoic Acid Signaling During Gastrulation Induces Developmental Microcephaly.Frontiers in cell and developmental biology · 2022Article
- Loss of tumor protein 53 protects against alcohol-induced facial malformations in mice and zebrafish.Alcoholism, clinical and experimental research · 2021Article
- Embryonic ethanol exposure on zebrafish early development.Brain and behavior · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal Alcohol Spectrum Disorder (FASD) is caused by prenatal alcohol exposure, producing craniofacial, sensory, motor, and cognitive defects. FASD is highly prevalent in low socioeconomic populations, which are frequently accompanied by malnutrition. FASD-associated ocular pathologies include microphthalmia, optic nerve hypoplasia, and cataracts. The present study characterizes specific retinal tissue defects, identifies ethanol-sensitive stages during retinal development, and dissects the effect of nutrient supplements, such as retinoic acid (RA) and folic acid (FA) on ethanol-induced retinal defects. Exposure to pathophysiological concentrations of ethanol (during midblastula transition through somitogenesis; 2-24 h post fertilization [hpf]) altered critical transcription factor expression involved in retinal cell differentiation, and produced severe retinal ganglion cell, photoreceptor, and Müller glial differentiation defects. Ethanol exposure did not alter retinal cell differentiation induction, but increased retinal cell death and proliferation. RA and FA nutrient co-supplementation rescued retinal photoreceptor and ganglion cell differentiation defects. Ethanol exposure during retinal morphogenesis stages (16-24 hpf) produced retinal defects like those seen with ethanol exposure between 2 and 24 hpf. Significantly, during an ethanol-sensitive time window (16-24 hpf), RA co-supplementation moderately rescued these defects, whereas FA co-supplementation showed significant rescue of optic nerve and photoreceptor differentiation defects. Interestingly, RA, but not FA, supplementation after ethanol exposure could reverse ethanol-induced optic nerve and photoreceptor differentiation defects. Our results indicate that various ethanol-sensitive events underlie FASD-associated retinal defects. Nutrient supplements like retinoids and folate were effective in alleviating ethanol-induced retinal defects.
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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.