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Endogenous Metal-Binding Proteins in the Control of Zinc, Copper, Cadmium and Mercury Metabolism During Prenatal and Post-Natal Development

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Abstract

Livers of prenatal and neonatal animals contain high concentrations of metallothioneins, which appear to function in copper (Cu) and/or zinc (Zn) homeostasis. In the newborn of some species the hepatic metallothioneins contain only small amounts of copper and seem to control only the metabolism of zinc. Before intestinal closure in such species (e.g. the rat), copper absorption may be regulated by a specific copper-binding complex. Neonates of certain other species (e.g. the Syrian hamster) appear to lack this intestinal copper-complex and to regulate the metabolism of copper and zinc by the synthesis of hepatic metallothionein.

The intestinal copper-complex and hepatic metallothionein of the newborn rat provide immediately-available binding sites for cadmium (Cd) and mercury (Hg). The former limits the transport of these metals across the intestine, whilst the latter binds them by replacement of zinc.

Both cadmium and mercury inhibit the placental transport of zinc and copper and, when administered in mid-gestation are teratogenic, possibly because of their effects on these processes. Newborn rat pups, from dams dosed with cadmium in late gestation, are deficient in hepatic zinc-metallothionein and their gain in body weight is retarded.

Interference with transport processes in both the maternal intestine and placenta contribute to the susceptibility of the fetus at chronic exposure of the dam to cadmium.

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Webb, M. (1983). Endogenous Metal-Binding Proteins in the Control of Zinc, Copper, Cadmium and Mercury Metabolism During Prenatal and Post-Natal Development. In: Clarkson, T.W., Nordberg, G.F., Sager, P.R. (eds) Reproductive and Developmental Toxicity of Metals. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9346-1_28

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