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Copper in fetal and neonatal development.

L S Hurley, C L Keen, B Lönnerdal

    Ciba Foundation Symposium
    |January 1, 1980
    PubMed
    Summary
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    Copper is essential for development, but its metabolism is complex. Supplementing copper in mutant mice models corrected developmental issues and normalized copper levels, highlighting copper

    Area of Science:

    • Developmental Biology
    • Nutritional Biochemistry
    • Genetics

    Background:

    • Copper is vital for fetal and neonatal development, yet its metabolic pathways during this critical period remain unclear.
    • Genetic factors significantly influence an organism's dietary copper requirements.
    • Specific mouse mutants (quaking and crinkled) exhibit developmental phenotypes partially mirroring copper deficiency.

    Purpose of the Study:

    • To investigate the role of copper supplementation in ameliorating developmental abnormalities in mouse models with genetic defects in copper metabolism.
    • To explore the impact of copper on neurological development, skin, hair, and enzyme activity in specific mutant mice.
    • To examine the developmental timing of copper metabolism errors in these genetic models.

    Main Methods:

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    • Maternal dietary supplementation with copper during pregnancy and/or lactation in quaking (qk) and crinkled (cr) mice.
    • Assessment of neurological phenotypes (tremors), copper concentrations in the brain, skin, and hair.
    • Monitoring neonatal survival rates and hematological parameters (anemia).
    • Measurement of copper-zinc-superoxide dismutase (Cu-ZnSOD) activity in liver and hair.
    • Analysis of copper molecular distribution in rat intestine during the neonatal period.

    Main Results:

    • Copper supplementation significantly reduced tremors in qk mice and normalized brain copper levels.
    • Prenatal copper supplementation improved neonatal survival and skin/hair development in cr mice.
    • cr/cr mice exhibited transient anemia and altered copper levels in liver and hair, which were normalized by supplementation.
    • Copper supplementation restored normal Cu-ZnSOD activity in cr mice, despite initial low levels.
    • Rat intestinal copper distribution showed drastic changes during the neonatal period, supporting rapid metabolic shifts.

    Conclusions:

    • Copper supplementation can effectively correct specific developmental defects and metabolic imbalances in mouse models with genetic mutations affecting copper utilization.
    • The genetic mutations in qk and cr mice impact copper metabolism at different developmental stages.
    • Rapid changes in copper metabolism occur during the neonatal period, underscoring the dynamic nature of copper homeostasis.