Most cases of congenital spinal
deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal
deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal
vitamin A deficiency and the production of congenital spinal
deformities in the offsping. Thirty two female rats were randomized into two groups: control group, which was fed a normal diet;
vitamin A deficient group, which were given
vitamin A-deficient diet from at least 2 weeks before mating till delivery. Three random neonatal rats from each group were killed the next day of parturition. Female rats were fed an AIN-93G diet sufficient in
vitamin A to feed the rest of neonates for two weeks until
euthanasia. Serum levels of
vitamin A were assessed in the adult and filial rats. Anteroposterior (AP) spine radiographs were obtained at week 2 after delivery to evaluate the presence of the skeletal abnormalities especially of spinal
deformities. Liver and vertebral body expression of
retinaldehyde dehydrogenase (RALDHs) and RARs
mRNA was assessed by reverse transcription-real time PCR. VAD neonates displayed many skeletal malformations in the cervical, thoracic, the pelvic and sacral and limbs regions. The incidence of congenital
scoliosis was 13.79% (8/58) in the filial rats of
vitamin A deficiency group and 0% in the control group. Furthermore,
vitamin A deficiency negatively regulate the liver and verterbral body
mRNA levels of RALDH1, RALDH2, RALDH3, RAR-α, RAR-β and RAR-γ.
Vitamin A deficiency in pregnancy may induce congenital spinal
deformities in the postnatal rats. The decreases of RALDHs and RARs
mRNA expression induced by
vitamin A deprivation suggest that vertebral
birth defects may be caused by a defect in RA signaling pathway during somitogenesis.