Birth defects research · 2026
Effects of Vitamin B12, Folic Acid, and L-Carnitine on Congenital Malformations Induced by Vitamin A Hypervitaminosis.
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Açık İlayda, Gökçimen Alpaslan, Kalkan Nur Sevim
Аннотация
BACKGROUND: Excessive intake of exogenous vitamin A during pregnancy has been associated with congenital malformations. This experimental study aimed to evaluate whether vitamin B12, folic acid, and L-carnitine exert a protective or contributory effect on malformations induced by hypervitaminosis A.
METHODS: Thirty-five healthy adult female Wistar albino rats and seven male rats were used. Pregnant rats received vitamin A alone or in combination with vitamin B12, folic acid, or L-carnitine for 21 consecutive days (GD 0-21). At the end of gestation, neonates were evaluated for gross congenital malformations. Brain, liver, and eye tissues were excised and processed for histopathological and morphometric analyses.
RESULTS: No gross external malformations were observed in any group; however, significant growth restriction and multi-organ histopathological alterations were detected in the offspring. Histological examination revealed interstitial edema in brain tissue and retinal detachment in the eye. Hepatic alterations included sinusoidal dilatation, hyperchromatic nuclei, necrotic cells, and cytoplasmic degenerative changes; these lesions remained mild. Somatic and organ morphometry showed that vitamin B12 supplementation partially alleviated retinoid-induced somatic growth retardation.
CONCLUSION: Although maternal hypervitaminosis A did not cause overt external malformations under the tested regimen, it induced multi-organ histopathological damage and severe fetal growth restriction. Adjuvant supplementation, particularly with vitamin B12, demonstrated modulatory effects against retinoid-induced developmental suppression.
METHODS: Thirty-five healthy adult female Wistar albino rats and seven male rats were used. Pregnant rats received vitamin A alone or in combination with vitamin B12, folic acid, or L-carnitine for 21 consecutive days (GD 0-21). At the end of gestation, neonates were evaluated for gross congenital malformations. Brain, liver, and eye tissues were excised and processed for histopathological and morphometric analyses.
RESULTS: No gross external malformations were observed in any group; however, significant growth restriction and multi-organ histopathological alterations were detected in the offspring. Histological examination revealed interstitial edema in brain tissue and retinal detachment in the eye. Hepatic alterations included sinusoidal dilatation, hyperchromatic nuclei, necrotic cells, and cytoplasmic degenerative changes; these lesions remained mild. Somatic and organ morphometry showed that vitamin B12 supplementation partially alleviated retinoid-induced somatic growth retardation.
CONCLUSION: Although maternal hypervitaminosis A did not cause overt external malformations under the tested regimen, it induced multi-organ histopathological damage and severe fetal growth restriction. Adjuvant supplementation, particularly with vitamin B12, demonstrated modulatory effects against retinoid-induced developmental suppression.