Zinc supplementation in ethanol-treated pregnant rats increases the metabolic activity in the fetal hippocampus.
As a possible preventative measure for brain dysfunction in the fetal alcohol syndrome, the effect of zinc supplementation together with ethanol on the fetal cerebrum, especially the hippocampus, was investigated. Female rats of an ethanol group and a control group received 30% ethanol and water, respectively. During pregnancy half of both groups received 0.01% zinc together with ethanol or water. Fetuses on gestational day 21 were examined biochemically and ultrastructurally. Administration of zinc with ethanol resulted in an increased cerebral weight and cerebral RNA content compared to administration of ethanol alone. However, these better results did not reach those of controls without ethanol. In the cytoplasm of hippocampal neurons from dams only given zinc with ethanol confronting cisternae were frequently observed between the rough endoplasmic reticulum and the rough endoplasmic reticulum or the nuclear envelope. Although the functional roles of the confronting cisternae were not definite, it is reasonable to conclude that the confronting cisternae were a repair mechanism of zinc against the inhibitory effect on RNA and protein syntheses of ethanol. This study shows evidence of prevention of the brain dysfunction on ethanol treatment.
D000818:Animals; D001923:Brain Chemistry; D004247:DNA / Q000032:analysis; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D006624:Hippocampus / Q000648:ultrastructure*; D007935:Leucine-tRNA Ligase / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000032:analysis; D011247:Pregnancy; D012313:RNA / Q000032:analysis; D051381:Rats; D015032:Zinc / Q000627:therapeutic use*
D009419:Nerve Tissue Proteins; D012313:RNA; D004247:DNA; D007935:Leucine-tRNA Ligase; D015032:Zinc