Prevention possibility for brain dysfunction in rat with the fetal alcohol syndrome--low-zinc-status and hypoglycemia.

As a treatable cause of CNS dysfunctions in the fetal alcohol syndrome (FAS), low-zinc-status in addition to hypoglycemia has been investigated in experimental rat models. During the premating period female rats of an ethanol group and a control group received 30% ethanol (E) and water (W), respectively. During pregnancy, some of both groups received zinc or nicotinamide-adenine dinucleotide (NAD) or nicotinamide throughout pregnancy and glucose for gestational day (gd) 15 to 19 with E or W. Independent of maternal blood glucose levels, maternal insulin levels were lower on gd 15 and 18 in the ethanol group than in the control one. A decrease in the activity of carbonic anhydrase in the hippocampal area on postnatal day (pd) 1 was observed in the ethanol group. Administration of zinc with E resulted in a better effect on fetal total body weight and on preventing resorption, mean fetal body weight and protein content in the cerebrum than administration of E alone. Administration of glucose only in the late gestational period resulted in a better effect on fetal cerebral weight than administration of E alone, with a decrease in the litter size. Administration of zinc with E during pregnancy resulted in higher maternal serum zinc levels, without an increase in fetal cerebral zinc content, than administration without zinc with E. There was a positive correlation between fetal body ethanol levels and maternal blood ethanol levels, and a negative correlation between fetal body ethanol levels and fetal total body weight. The beneficial effect of supplementary zinc on fetal growth may possibly help preventing the CNS dysfunctions of FAS, but it is important that the effect was not good compared to the control without E.