Added Dietary Inorganic Sulfate and Its Effect upon Rats Fed Molybdenum

Miller, R. F.; Price, N. O.; Engel, R. W.

doi:10.1093/jn/60.4.539

Cited by 44 publications

(11 citation statements)

References 9 publications

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“…The ability of dietary Mo to raise the Cu and Mo concentrations of the liver of rats has been demonstrated before (Miller et al 1956;Brinkman et af. 1961 ;Mills & Mitchell, 1971).…”

Section: Discussionmentioning

confidence: 91%

“…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 1968; Suttle & Field, 1968;Smith & Wright, 1g75a, b;, a reduced transport of @Cu from the blood to the liver after intravenous injection (Smith et al 1968;Marcilese et al 1969) and a continuously increased plasma Cu concentration when high doses of Mo are given orally (Bingley, 1974). The same observations have been made as a consequence of Mo feeding in non-ruminants: an increased plasma Cu concentration in rats (Miller et al 1956), a plasma Cu fraction in guinea-pigs that is insoluble in trichloric acid (Suttle, 1973;Smith & Wright, 1975 b) and a reduced transport of 64Cu from blood to liver in rat (Compke et al 1969, rabbit (Gaballah, Abood, Caleed et al 1965) and pig (Standish 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.…”

mentioning

confidence: 72%

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

Nederbragt

1980

Br J Nutr

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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.

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“…The ability of dietary Mo to raise the Cu and Mo concentrations of the liver of rats has been demonstrated before (Miller et al 1956;Brinkman et af. 1961 ;Mills & Mitchell, 1971).…”

Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 72%

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

Nederbragt

1980

Br J Nutr

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“…Miller et al 48 studies the effect of two doses of molybdenum in the diet (75 and 300 mg Mo kg Ϫ1 day Ϫ1 on the skeletal system and growth of rats exposed for only 6 weeks. Even for this short period, the study is well done and the results are clear.…”

Section: Animal Studiesmentioning

confidence: 99%

Assessment of molybdenum toxicity in humans

Vyskočil¹,

Viau²

1999

J. Appl. Toxicol.

196

112

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In an attempt to define a tolerable daily intake (TDI) for molybdenum based on a toxicological risk analysis approach, a large literature survey was conducted. In man, absorption of molybdenum after oral intake is in the range of 28–77% and urinary excretion is 17–80% of the total dose. A low order of toxicity of molybdenum compounds has been observed in humans. However, with the available data, it is not possible to calculate any dose–response or dose–effect relationships. Because molybdenum toxicity is associated with copper intake or depleted copper stores in the body, humans who have an inadequate intake of dietary copper or some dysfunction in their copper metabolism that makes them copper‐deficient could be at greater risk of molybdenum toxicity. In the absence of relevant human studies, animal studies were evaluated for the derivation of the TDI. Effects of Mo on reproduction and foetal development were found to be critical effects observed in rats and mice. A dose–response relationship was observed in a study by Fungwe et al., with a ‘no observed adverse effect’ level (NOAEL) and a ‘lowest observed adverse effect’ level (LOAEL) of 0.9 and 1.6 mg Mo kg−1 day−1, respectively. Applying uncertainty factors of 10 for intraspecies and 10 for interspecies differences to the NOAEL, a TDI of 0.009 mg Mo kg−1 day−1 was calculated. The TDI is given a medium confidence rating. This TDI is more than double the upper limit of adequate intake for adolescents and adults that was derived from the Mo content of the average diet in the USA. Copyright © 1999 John Wiley & Sons, Ltd.

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“…T his is in con tr a s t to th e w o rk o f M iller et al [9] w ho fo u n d t h a t feeding excess m o ly b d en u m (100 p p m d ie ta ry Mo as N a 2 M o04 .2 H 20 for 6 weeks) to r a ts re su lte d in e le v a te d liv e r levels o f Cu and Mo a n d to B rin k m a n et al [1] w ho o b serv ed th a t th e d ie ta ry a d m in istra tio n o f N a 2M o 0 4 . 2 H 20 a t levels o f 200, 300 a n d 400 p p m to ra ts for 6 w eeks increased th e Cu level in th e liv er cell nuclei a n d d eb ri and in th e m ito ch o n d ria.…”

Section: R Esults a Nd Discussionmentioning

confidence: 97%