It is thought that 5-10% of human serum
copper consists of
copper ions complexed with
histidine,
amino acids or
albumin. The
phenanthroline assay developed by Gutteridge (Biochem. J. 218, 983-985; 1984) is shown to measure all these forms of
copper down to a sensitivity of 0.1 mumol/dm3, yet it does not detect any
copper ions in freshly-prepared serum or plasma from rats, mice, rabbits or guinea-pigs, or freshly-prepared serum from humans. It is concluded that the "non-
caeruloplasmin copper pool" is much smaller than has previously been supposed. No
phenanthroline-detectable
copper could be measured in serum freshly prepared from four patients with uncomplicated
Wilson's disease, but it could be measured in serum from a patient with
fulminant hepatic failure. After
liver transplantation, concentrations of
phenanthroline-detectable
copper in this patient fell to zero within two days. Studies on the
ferroxidase activity of freshly-prepared serum or plasma samples shows that little
ferroxidase II activity is present in samples from healthy adults or from the patient with
Wilson's disease and
fulminant hepatic failure. In all the patients,
ferroxidase I activities are sub-normal. Freshly-prepared plasma or serum samples from several animal species generally show lower
ferroxidase I and greater
ferroxidase II activities than do human samples, but only in rabbits does
ferroxidase II account for a high proportion of total plasma
ferroxidase activity. Storage of
biological fluids can cause release of
copper from
caeruloplasmin and a rise in
ferroxidase II activity; these events may have confused some earlier studies.