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Published on: November 20, 2015
Prenatal vitamin A deficiency causes laryngeal malformation in rats
Ichiro Tateya1, Tomoko Tateya, Rebecca Lynn Surles
1Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Insights
Vitamin A deficiency in pregnant rats led to significant laryngeal and vocal fold developmental defects in offspring. This highlights vitamin A
Area of Science:
- Developmental Biology
- Teratology
- Nutritional Science
Background:
- Previous research suggests a link between vitamin A and vocal fold development.
- Understanding the role of essential vitamins in prenatal development is crucial for preventing congenital abnormalities.
Purpose of the Study:
- To investigate the impact of vitamin A deficiency on prenatal laryngeal development in a rat model.
- To determine if post-embryonic day 11 vitamin A deficiency affects laryngeal formation.
Main Methods:
- A rat model was developed to induce vitamin A deficiency after embryonic day 11.
- Pregnant rats (5 deficient, 5 control) were studied.
- Embryos were collected at embryonic day 18.5 and analyzed histologically for laryngeal development.
Main Results:
- Vitamin A-deficient embryos exhibited a 18% survival rate.
- Observed malformations included laryngotracheal cartilage defects, incomplete glottis separation, and laryngoesophageal clefts.
Conclusions:
- Vitamin A plays a critical role in normal prenatal laryngeal and vocal fold development.
- Deficiency during specific developmental windows can lead to severe congenital malformations.
Objectives:
Our previous research demonstrated that vitamin A might be related to vocal fold development. The purpose of this study was to determine whether vitamin A deficiency affects prenatal laryngeal development in rats.
Methods:
Two considerations were necessary in designing a study using a rat model: for embryonic survival, vitamin A is necessary through day 10 of gestation, and laryngeal formation occurs primarily after day 11. Thus, we created a rat model that developed vitamin A deficiency after embryonic day 11. Ten pregnant rats (5 vitamin A-deficient rats and 5 control rats) were studied. Embryos were collected at embryonic day 18.5 and analyzed histologically.
Results:
Eighteen percent of the vitamin A-deficient embryos were alive and demonstrated laryngotracheal cartilage malformation, incomplete separation of the glottis, and/or laryngoesophageal clefts.
Conclusions:
These results document the important role played by vitamin A in laryngeal development.
