Abstract
Zinc is essential for normal embryonic growth and differentiation. A high rate of fetal neural tube defects occurs in pregnancies of women with untreated acrodermatitis enteropathica and in experimental gestational zinc deficiency in rats; however, serum zinc is normal in children with spina bifida and in mothers of anencephalics during gestation. Confluent cultures of skin fibroblasts from two term newborns with anencephaly and lumbar meningomyelocele and three age-matched controls were studied in triplicate in six experiments. 65ZnC12 (2 μCi, 55 nM Zn++, 2 × 105 cells) was added in fresh media (10% horse serum) and counted in whole washed cell suspensions at 24 hours. 65Zn uptake was significantly (p < .001) lower in the infants with neural tube defects (281 ±9.5 cpm/μg DNA) compared to controls (382 ±50.7). The rate of zinc uptake was repeatable in each cell line. These results may reflect an abnormality of cellular zinc metabolism in infants with neural tube defects. We postulate that depressed embryonic uptake of zinc, perhaps due to heritable regulatory mechanisms, limits cellular differentiation during critical periods and thereby contributes to defective CNS formation.
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Zimmerman, A., Rowe, D., Stover, M. et al. 1226 DEPRESSED CELLULAR ZINC UPTAKE IN ANENCEPHALY AND SPINA BIFIDA. Pediatr Res 15 (Suppl 4), 647 (1981). https://doi.org/10.1203/00006450-198104001-01252
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DOI: https://doi.org/10.1203/00006450-198104001-01252