Early retinoic acid deprivation in developing zebrafish results in microphthalmia
Open accessAbstract
Vitamin A deficiency causes impaired vision and blindness in millions of children around the world. Previous studies in zebrafish have demonstrated that retinoic acid (RA), the acid form of vitamin A, plays a vital role in early eye development. The objective of this study was to describe the effects of early RA deficiency by treating zebrafish with diethylaminobenzaldehyde (DEAB), a potent inhibitor of the enzyme retinaldehyde dehydrogenase (RALDH) that converts retinal to RA. Zebrafish embryos were treated for 2 h beginning at 9 h postfertilization. Gross morphology and retinal development were examined at regular intervals for 5 days after treatment. The optokinetic reflex (OKR) test, visual background adaptation (VBA) test, and the electroretinogram (ERG) were performed to assess visual function and behavior. Early treatment of zebrafish embryos with 100 μM DEAB (9 h) resulted in reduced eye size, and this microphthalmia persisted through larval development. Retinal histology revealed that DEAB eyes had significant developmental abnormalities but had relatively normal retinal lamination by 5.5 days postfertilization. However, the fish showed neither an OKR nor a VBA response. Further, the retina did not respond to light as measured by the ERG. We conclude that early deficiency of RA during eye development causes microphthalmia as well as other visual defects, and that timing of the RA deficiency is critical to the developmental outcome.
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Electroretinogram (ERG) measurements indicate that DEAB treated 5.5 dpf zebrafish exhibited null levels of electrical responses in response to a light stimulus when compared to non-treated zebrafish.
“Additionally, electroretinogram (ERG) measurements indicate that DEAB treated 5.5 dpf zebrafish exhibited null levels of electrical responses in response to a light stimulus when compared to non-treated zebrafish [51].”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [51]
The Results section reports that ERG recordings at 5.5 dpf showed no components in DEAB-treated larvae, while controls had typical responses. However, the Discussion notes that a small group of DEAB-treated larvae without microphthalmia had reduced, rather than absent, ERG amplitudes. The unqualified claim therefore overstates the result for all treated larvae. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn the DEAB experiment, treated zebrafish exhibited impaired retinal development in the 36, 60, 84 hpf larval stages and significant microphthalmia at the 5.5 dpf stage.
“In the DEAB experiment, treated zebrafish exhibited impaired retinal development in the 36, 60, 84 hpf larval stages and significant microphthalmia at the 5.5 dpf stage.”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [51]
DEAB induced impaired development of the eye in zebrafish models.
“One of the Raldh chemical inhibitors used in John Dowling’s work includes diethylaminobenzaldehyde (DEAB), which induced impaired development of the eye in zebrafish models [51].”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [51]
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- Authors
- LE, H.-G. T., DOWLING, J. E., & CAMERON, D. J.
- Affiliations
- Harvard University (US)
- Corresponding author
- CAMERON, D. JOSHUA
- Venue
- Visual Neuroscience
- Publisher
- Maximum Academic Press
- Published
- 2012-09
- Volume
- 29
- Issue
- 4-5
- Pages
- 219-228
- ISSN
- 0952-5238 (ISSN-L)
- 1469-8714
- PMC
- PMC3718850
- OpenAlex
- W2144411483
- Cited by
- 46
- References
- 46
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 8 · 2020: 2 · 2019: 4 · 2018: 1 · 2017: 1 · 2015: 7 · 2014: 3 · 2013: 3
- FWCI
- 1.67
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Visual Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Western University of Health Sciences
- National Institutes of Health
- National Eye Institute (T32 EY 07145, R01EY000811, EY000811, T32EY007145)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Ocular Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- microphthalmia, zebrafish eye development, vitamin A deficiency, visual function, optokinetic response, electroretinogram, retinal lamination
- MeSH terms
- Adaptation, Ocular, Animals, Behavior, Animal, Electroretinography, Embryo, Nonmammalian, Eye, Larva, Microphthalmos, p-Aminoazobenzene, Phenotype, Reflex, Tretinoin, Vitamin A Deficiency, Zebrafish, Nystagmus, Optokinetic
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