Abstract
Alcoholism has adverse effects on zinc (Z) nutrition. We postulate that Z deficiency is synergistic with ethanol (E) in the fetal alcohol syndrome (FAS). We compared the effects of E on progeny of pregnant mice fed a Z deficient diet compared to a diet with high Z. Pregnant CBA mice (n=66) were fed the Lieber-DeCarli liquid diet with 0%, 157, or 20% E containing .3 (L) or 8 (H)μg/ cc Z. Dams were sacrificed on day 18 of gestation. Number of implantations (Imp), resorptions (Res), fetal (F) wt., and external malformations were recorded. Fetal Z and Z metalloenzymes, soft tissue anomalies, and skeletal malformations were assessed.
Fetal weights were lower in the groups fed the Z deficient diet for each concentration of E (p<.005). The groups fed the combination of low Z plus E had 37-52% res, while the animals on the Z deficient diet without E or the high Z diet with E had 0-2% res. Skeletal malformations were related to E concentration but not Z intake, while soft tissue anomalies were higher in those maintained on the low Z-E diet. These results suggest that Z deficiency potentiated the teratogenic effects of E and that nutritional intervention might reduce the incidence or severity of FAS.
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Keppen, L., Pysher, T. & Rennert, O. 1298 ZINC DEFICIENCY POTENTIATES ETHANOL EMBRYOPATHY. Pediatr Res 19, 327 (1985). https://doi.org/10.1203/00006450-198504000-01322
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DOI: https://doi.org/10.1203/00006450-198504000-01322