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The maternal combined supplementation of folic acid and Vitamin B(12) suppresses ethanol-induced developmental toxicity in mouse fetuses.

Reproductive Toxicology (Elmsford, N.y.)

therapeutic use, Abnormalities, Drug-Induced, blood, administration & dosage, Vitamin B 12, Pregnancy, Mice, drug effects, Homocysteine, Gestational Age, Folic Acid, prevention & control, chemically induced, Fetal Growth Retardation, Fetal Development, Female, toxicity, antagonists & inhibitors, Ethanol, Embryo Loss, Embryo Implantation, Dietary Supplements, embryology, abnormalities, Bone and Bones, Animals, etiology, Alcoholic Intoxication

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      Abstract

      Maternal ethanol consumption during pregnancy can induce developmental defects in the fetus. The objective of this study was to assess whether combined supplementation of folic acid (FA) and Vitamin B(12) (VB(12)) in dams would suppress ethanol-induced developmental toxicity in CD-1 mice. Ethanol (5.0 g/kg) was given intragastrically from gestational day (GD) 6 to GD15. Vitamin supplementation groups were additionally given 60.0 mg/kg FA, 1.0 mg/kg VB(12), or 60.0 mg/kg FA+1.0 mg/kg VB(12) during GD1-16. The control group received distilled water only. Results of litter evaluation on GD18 showed that combined supplementation of FA and VB(12) ameliorated many of the adverse effects of ethanol. In contrast, the single vitamin supplementation groups showed little or no amelioration. These results suggest that combined supplementation of FA and VB(12) was more effective than each vitamin toward suppressing ethanol-induced developmental toxicity in CD-1 mice.

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      Journal
      10.1016/j.reprotox.2005.12.004
      16439097

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