"August 2002" / Bibliography: leaves 141-176. / ix, 179 leaves : ill. (some col.) ; 30 cm / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Changes 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. / Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2003