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dc.contributor.authorCarey, Luke Charlesen
dc.description"August 2002"en
dc.descriptionBibliography: leaves 141-176.en
dc.descriptionix, 179 leaves : ill. (some col.) ; 30 cmen
dc.description.abstractChanges in maternal-foetal zinc homeostasis resulting in a foetal deficiency may be an important contributing factor in ethanol-realted teratogenicity. Ethanol induces expression of hepatic metallothionein, causing zinc transfer from the plasma to the liver. Rodent studies show that changes in plasma zinc correlate with a high incidence of abnormal fetuses in MT+/+ mice. Demonstrates a clear link between maternal hepatic MT induction, decreased foetal zinc supply, and teratogenicity, which has major implications for binge alcohol consumption in early pregnancy. The demonstration that zinc treatment is effective in preventing teratogenicity indicates potential treatment strategies.en
dc.format.extent71377 bytesen
dc.subject.lcshFetal alcohol syndrome Animal models.en
dc.subject.lcshZinc in the body Animal models.en
dc.subject.lcshAlcohol Toxicology Animal models.en
dc.subject.lcshMetallothionein Physiological effect Animal models.en
dc.titleEthanol teratogenicity : the aetiological importance of zinc and metallothionein / by Luke Charles Carey.en
dc.contributor.schoolDept. of Physiologyen
dc.provenanceThis electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exception. If you are the author of this thesis and do not wish it to be made publicly available or If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at:
dc.description.dissertationThesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2003en
Appears in Collections:Research Theses

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