Published online by Cambridge University Press: 09 March 2007
1. Male WAG/Cpb inbred rats fed on rations containing 1·5 mg copper/kg (deficient) and 6·0 mg Cu/kg (adequate) were supplemented with molybdenum (500 mg/kg diet). Starting at week 0 rats were killed weekly for up to 6 weeks and the caeruloplasmin activity of plasma, the Cu concentration of plasma, liver and kidney and the Mo concentration of liver and kidney were determined. The experiment was repeated with rats fed on diets of the same composition but given additional Cu for periods of 2 weeks. Cu was given orally by increasing dietary Cu to 6·0 mg/kg and 25·0 mg/kg for Cu-deficient and Cu-adequate rats respectively or intraperitoneally by injecting 75 μg and 250 μg every second day to Cu-deficient and Cu-adequate rats respectively.
2. After Mo administration to Cu-deficient rats plasma and kidney Cu and liver and kidney Mo increased but caeruloplasmin activity and liver Cu decreased. In Cu-adequate rats plasma, liver and kidney Cu and liver and kidney Mo increased to much higher levels than in Cu-deficient rats. Caeruloplasmin activity was not affected. Fluctuations in plasma Cu and kidney Mo were correlated closely.
3. No qualitative difference between the effect of oral or intraperitoneal Cu administered to Mo-treated Cu-deficient or Cu-adequate rats was found. In Cu-deficient Mo-supplemented rats additional Cu increased plasma Cu, caeruloplasmin activity and liver and kidney Cu and Mo. In Cu-adequate Mo-supplemented rats additional Cu decreased plasma Cu and liver and kidney Mo and increased caeruioplasmin activity and kidney Cu and, to a minor extent, liver Cu.
4. In view of the assumption that in rats a Cu, Mo and S containing compound, related to Cu-thiomolybdate, may be formed in vivo the results suggest thai Cu binds to the Mo-S part of the compound; when this compound is formed in the gastro-intestinal tract it can not be absorbed and when it is formed at systemic sites it changes the Cu distribution.