Fetal Alcohol Syndrome in Rats: Conditions for Improvement of Ethanol Effects on Fetal Cerebral Development with Supplementary Agents

Abstract

As a possible preventative measure for brain dysfunction in the fetal alcohol syndrome, the effect of zinc or vitamin E supplementation together with ethanol on the fetal cerebrum was investigated in rats. Contrary to our previously published data showing the good effect of 0.01% zinc with 30% ethanol on fetuses, the administration of 0.01% zinc with 20% ethanol, 0.03% vitamin E with 20% ethanol or 0.02% vitamin E with 10% ethanol during pregnancy did not result in a good effect on the body and cerebral weights of fetuses on gestational day 21. The development of dendritic branches on frontal cerebral neurons in fetuses was decreased in the order of the control, zinc with ethanol and ethanol groups. The concentration and content of α-tocopherol were increased, but those of zinc were not, in the fetal cerebrum with the maternal administration of vitamin E or zinc together with ethanol, respectively. These results suggest that the improvement of the brain function might depend on the deficient agent induced by maternal ethanol ingestion.

Dietary Zinc Supplementation Throughout Pregnancy Protects Against Fetal Dysmorphology and Improves Postnatal Survival After Prenatal Ethanol Exposure in Mice

“…That no consistent benefits have been reported using Zn supplementation in chronic ethanol studies (Keppen et al., 1990; Tanaka et al., 1982, 1983, 1988) would suggest that a non‐Zn‐related etiology(s) is responsible for the fetal dysmorphology when exposure is prolonged. Moreover, the timing of ethanol exposure during pregnancy may be critical to the mechanism that underpins the damage to the fetus.…”

Zinc Supplementation at the Time of Ethanol Exposure Ameliorates Teratogenicity in Mice

“…Keppen et al (1990) found that pregnant mice fed a liquid diet containing ethanol with supplemental Zn (four times the recommended daily allowance) had fetuses that were not different from the nonsupplemented group in terms of developmental defects. However, experimentation in the laboratory of Tanaka, where pregnant rats were given excess Zn in the diet, have demonstrated both positive (Tanaka et al, 1982) but mostly negative effects (Tanaka et al, 1988;Tanaka, 1998) of supplementation.…”

The Role of Oxidative Stress in Spontaneous Abortion and Recurrent Pregnancy Loss: A Systematic Review

“…Heavy alcohol intake during pregnancy can result in fetal alcohol syndrome and its incidence is estimated to be high in the developed world. It has been proposed that antioxidant supplementation will overcome ethanol-induced ROS production and decrease fetal damage (88,89). Ascorbic acid has been shown to inhibit alcohol mediated generation of ROS in embryos of Xenopus laevis and prevented microencephaly and intrauterine growth retardation in ethanol-exposed embryos (90).…”