Abstract
The X-linked mouse mutant brindled is a model for Menkes syndrome. In young hemizygotes, reduced liver and brain copper concentrations are associated with neurologic dysfunction. In fetuses copper concentrations in placenta and kidney are higher in brindled than controls while those in liver and carcass are lower. To treat the copper deficiency in brindled young, heterozygotes were injected at 16 or 18 days gestation with copper, 6 mcg/g/dose, as cupric chloride, 18 and 6 hours before sacrifice. Placental, carcass, and hepatic copper concentrations in brindled fetuses increased (p>0.006). Injection of methylprednisolone, 5 mcg/g, 20 hours before the copper, to increase fetal hepatic copper storage through metallothionein induction, resulted only in further increase in the carcass copper concentrations. These data suggest: placental copper transport in brindled fetuses is impaired; hepatic copper binding capacity of control and brindled fetuses is limited and cannot be augmented by pretreatment with methylprednisolone; extra-hepatic copper binding may be increased with methylprednisolone, which implicates induction of extra-hepatic metallothionein in both groups of animals.
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Garnica, A., Bates, J. & Rennert, O. PLACENTAL COPPER TRANSPORT IN THE BRINDLED MOUSE. Pediatr Res 21 (Suppl 4), 290 (1987). https://doi.org/10.1203/00006450-198704010-00735
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DOI: https://doi.org/10.1203/00006450-198704010-00735