Copper in fetal and neonatal development.

The essentially of copper for normal fetal and neonatal development has been well documented, although copper metabolism during this period is poorly understood. The dietary requirement for copper is influenced by genetic background. The neurological phenotypic characteristics of the mutant gene quaking (qk) in mice resemble in part those of copper-deficient animals. Supplementation of the maternal diet with copper during pregnancy and lactation, or during lactation alone, greatly reduced the frequency of tremors characteristic of these mutants, and brought the otherwise low copper concentrations in the brain to normal. Prenatal copper supplementation of crinkled (cr) mice increased neonatal survival and produced nearly normal development of skin and hair. Non-supplemented cr/cr mice showed anaemia at 21 days of age which disappeared later. Similarly, copper concentration in liver and hair was low in young but normal in old cr/cr mice. However, activity of copper--zinc-superoxide dismutase (Cu-ZnSOD) remained low even at 60 days of age. Copper supplementation brought both SOD activity and copper concentration of liver and hair to normal. The errors in copper metabolism produced by qk and cr appear to be expressed at different periods of development. The hypothesis that there are rapid changes in the metabolism of copper is supported by the observation that molecular distribution of copper in rat intestine changes drastically during the neonatal period.