PubMed · 5962739
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T Kawai. 1966. [Ceruloplasmin].. https://pubmed.ncbi.nlm.nih.gov/5962739/
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Copper uptake from copper-dihistidine complexes by microvillar vesicles from human placenta was studied. Uptake occurred in two phases: a rapid initial binding followed by approximately linear uptake to equilibrium at approximately 5 min. The uptake showed temperature dependence, was saturable (apparent Vmax 10.5 +/- 1.6 nmol/(mg protein.4 min), apparent Km of 0.6 +/- 0.12 mumol/L) and decreased with increasing osmotic pressure, showing that the Cu uptake arose from accumulation within the vesicles and not from extravesicular binding or isotope exchange. Ceruloplasmin blocked uptake of 64Cu from 64Cu-dihistidine by the vesicles, with 50% inhibition achieved at a protein concentration of 5-10 mumol/L and a 64Cu-dihistidine concentration of 1.5 mumol/L. The effect was specific, because glucose oxidase, a noncopper protein, increased apparent uptake by binding copper and in turn being bound to the nitrocellulose membranes used to separate vesicles from incubation medium. Adding increasing concentrations of histidine also decreased uptake. The data presented indicate that the placenta can accumulate copper from copper-dihistidine, that ceruloplasmin can interfere with uptake and that this system will be very valuable in elucidating the first stage in transfer of copper across the placenta.
We report a male infant with Menkes' disease who showed, at the age of 3 months, slow growth, hair abnormalities such as pili torti and white hair, and low levels of serum copper and ceruloplasmin. The exceptionally bright portions of his hair contained eumelanin and pheomelanin at levels only half those of normal Japanese controls. After subcutaneous administration of copper-histidinate for 2 months, his scalp hair changed to dark brown.