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

Tanaka, Harumi; Nakazawa, Kazuharu; Suzuki, Norihiro; Arima, Masataka

doi:10.1016/s0387-7604(82)80070-3

Cited by 25 publications

(14 citation statements)

References 19 publications

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“…The fetal body weight after cesarean sec tion and fetal cerebral weight 1 h after cesar ean section are shown in table II, compared with in the previous study [1], Because of the different conditions of each experiment after birth, the sources for cerebral weight mea surements were as follows; cerebrum from Values are expressed as p. compared to the corre sponding mean weights of fetuses from dams receiv ing water. Chronic = Before mating and during preg nancy; acute = during pregnancy.…”

Section: Resultsmentioning

confidence: 95%

“…The finding of the interrelationship be tween FAS and zinc or the hippocampus led to the attractive hypothesis that zinc nutri tion plays an important role in the pathogen esis of FAS, as discussed in our previous papers [1,2]. The manifestation of fetal dysmorphogenesis in alcoholic women appears to be related to the low zinc status of mater nal plasma [12].…”

Section: Discussionmentioning

confidence: 92%

“…The rat FAS model was produced essentially as described previously [1,5,6]. To get mothers ethanol tolerant before mating, ethanol drinking was induced for more than 1 month, because by this time a rat that did not tolerate ethanol had died.…”

Section: Methodsmentioning

confidence: 99%

“…In previous studies (table I), we demonstrated a good effect of 0.01 % zinc supplementation on fetuses from dams given 30% ethanol during pregnancy on a solid diet (4.2 mg zinc/100 g diet; F-2, Funabashi Corp., Chiba, Japan) ad libitum. There were increased body and cerebral weights, cerebral RNA and protein contents, and confronting cistemae between the rough endoplasmic reticulum and the rough endo plasmic reticulum or the nuclear enve lope in the cytoplasm of hippocampal neu rons [1,2]. These beneficial effects of supple mentary zinc on fetal cerebral development…”

mentioning

confidence: 95%

“…From our previous reports [1,2], may possibly help prevent the CNS dysfunc tions in FAS, however, the effect is limited and the level never reaches the control level without ethanol [1], Recent studies involving animal models of FAS have demonstrated the failure of zinc supplementation to reverse the effect of eth anol on the placental transport of zinc [3], and that zinc deficiency acts as a co-teratogen with alcohol [4], The present investiga tion was designed to clarify the limitation of the better effect of maternal ethanol inges tion with zinc, in comparison with the re sults of the previous studies. Furthermore, the placental transport of zinc with ethanol was discussed as compared to that of vita min E with ethanol.…”

mentioning

confidence: 99%

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

Tanaka¹,

Iwasaki²,

Nakazawa³

et al. 1988

Neonatology

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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.

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Section: Resultsmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 92%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 95%

mentioning

confidence: 99%

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

Tanaka¹,

Iwasaki²,

Nakazawa³

et al. 1988

Neonatology

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Fetal alcohol syndrome and DiGeorge anomaly. Critical ethanol exposure periods for craniofacial malformations as illustrated in an animal model

et al. 1986

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Acute maternal ethanl (alcohol) administration induces different craniofacial anomalies in the offspring of experimental animals, depending on the gestational day of teratogen exposure. Previous studies in our laboratories have illustrated the sequence of developmental changes leading to the "typical" fetal alcohol syndrome (FAS) craniofacial phenotype which results from teratogen exposure during gastrulation. These facial features are accompanied by deficiencies in median forebrain derivatives. Ethanol teratogenesis at this time apparently results in a loss of midline territory of the embryonic disc with little effect on neural crestdependent laterally derived structures including the visceral arches. Acute ethanol exposure in mice 1 1/2 days later, at a time when neural crest cells are populating the frontonasal prominence and the visceral arches, results in a craniofacial phenotype that is similar to that noted in the DiGeorge anomaly or sequence. Sequential scanning electron microscopic analysis in our laboratory of embryos exposed on day 8 1/2 have illustrated deficiencies in the developing facial prominences and the visceral arches. The developing forebrain and midbrain appear hypoplastic. We have also observed heart, great vessel, and thymus abnormalities in these fetuses. Histologic analyses indicate that a common pathogenetic basis for the above-mentioned (day 8 U2-induced) fetal alcohol effects appears to be an interference with the integrity of the cranial (including occipital) neural crest. Other discrete cell populations may also be involved since we have observed abnormalities in other regions, including placodal and closing membrane tissues. Sulik et a1This animal model provides evidence linking maternal ethanol abuse during the 3rd or 4th weeks of human gestation to the development in the conceptus of FAS or DiGeorge anomally craniofacial characteristics, respectively. As the DiGeorge anomaly has been noted in the offspring of alcoholic women, this animal model indicates that ethanol and/or its metabolites is, in these cases, the causative agent.

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Alcohol Abuse: Carcinogenic Effects and Fetal Alcohol Syndrome

Garro¹,

Gordon²,

Lieber³

1992

Medical and Nutritional Complications of Alcoholism

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

Cited by 25 publications

References 19 publications

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

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

Fetal alcohol syndrome and DiGeorge anomaly. Critical ethanol exposure periods for craniofacial malformations as illustrated in an animal model

Alcohol Abuse: Carcinogenic Effects and Fetal Alcohol Syndrome

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