The influence of molybdenum on the copper metabolism of the rat at different Cu levels of the diet

Abstract

1.Male WAG/Cpb inbred rats fed on rations with approximately 1-5 rng copper/kg (deficient), 6.0 mg Cu/kg (adequate) and 25.0 mg Cu/kg (excess) were supplemented with varying amounts of molybdenum (0, 50, 150 and 500 mg/kg diet) and the effect on the Cu concentration of blood, plasma, liver and kidney, the caeruloplasmin activity of plasma and the Mo concentration of liver and kidney were studied.2. M o increased the Cu concentration of blood, plasma, liver and kidney and the Mo concentration of liver and kidney. 3. In the plasma of Mo-supplemented rats the presence of a Cu-containing fraction was demonstrated, the Cu of which did not react with dithiocarbamate and was not related to caeruloplasmin. The Cu in this fraction was not able to increase the caeruloplasmin activity in the plasma of Cu-deficient Mo-supplemented rats. The Cu concentration of the erythrocytes did not seem to have been increased by the Mo treatment.4. When compared to Cu-adequate rats the effect of Mo on the Cu distribution was reduced both by Cu deficiency and Cu excess. This decreased effect of Mo was explained by reduced uptake or retention of MO in the body as observed in the liver and kidney.In both ruminants and single-stomached animals (non-ruminants) molybdenum alone or in combination with sulphate interacts with copper metabolism. In ruminants Mo decreases the Cu concentration of blood and liver, an effect that is enhanced by SO,. In non-ruminants the Cu concentration of blood and liver is increased by Mo, an effect that is counteracted by SO,. In ruminants the Cu-Mo interaction may be explained by the dominating role of microbial processes in the rumen at the Mo levels commonly used in ruminant diets; it is suggested that the microbial-mediated formation of Cu-thiomolybdate complexes in the rumen prevents Cu absorption (Suttle, 1974; Dick et al. 1975). However, in sheep it has been observed that Mo has some effects comparable to those in non-ruminants. These effects are: an increase in the free plasma Cu concentration and the presence of a 'tightly' bound, non-caeruloplasmin Cu fraction (Smith et al. . 1975). This resemblance in influence of Mo on systemic Cu in ruminants and non-ruminants suggests that the effect of Mo feeding in ruminants may be the result of two interactive processes of which the first may be found in the rumen and the second (comparable to that in nonruminants) in the tissues. It was the purpose of this study to investigate the systemic effect of Mo on Cu metabolism in more detail, using rats as an animal model.

Influence of ascorbic acid supplementation on copper status in young adult men

“…10 gm amount suggested byPauling (63). This study indicated that 1500 mg ascorbic acid daily over a relatively short period of time can significantly decrease copper status in healthy adult males.The results of this study call into question safety of prolonged self dosage of ascorbic acid at high levels.SUMMARYIntestinal absorption of copper has been found to be decreased in the presence of such factors as zinc,' molybdenum, cadmium and potassium sulfide(5)(6)(7)(8)(9). Findings from several animal studies indicate that ascorbic acid will also decrease intestinal copper absorption(10)(11)(12)(13)(14).…”

“…The effect of molybdenum may be due to its nonspecifically binding to sulfur compounds that are specific for copper(62). In the rat molybdenum was found to raise blood levels of molybdenum and copper when copper intake was adequate(9).…”

The effects of 3,3′,4,4′-tetrabromobiphenyl on rats fed diets containing a constant level of copper and varying levels of molybdenum

“…Molybdenum (Mo), also an essential trace element, is found in enzymes such as xanthine oxidase (Schwarz et al 2009). The metabolism of these two essential elements is interrelated so that an increase in dietary Mo can interfere with the bioavailability of Cu (Nederbragt 1980). This may be due to a decrease in Cu absorption and/or interference by Mo with Cu utilization.…”

Interaction of alkylmercuric compounds with sodium selenite. III. Biotransformation, levels of metallothioneinlike proteins and endogenous copper in some tissues of rats exposed to methyl or ethylmercuric chloride with and without sodium selenite.

“…Changes in the homeostasis of essential elements, especially zinc and copper, by toxic metals have been studied from the standpoint of understanding of the harmful action of the metals on the organism (1,2). Disturbances in the metabolism of endogenous metals may be induced in experimental animals by administration of cadmium (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17), nickel (3,18,19), silver (18,(20)(21)(22), bismuth (23,24), gold (25,27), tin (28), molybdenum (29), and both inorganic mercury (22,23,26,(30)(31)(32) and methylmercury (31).…”