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At least 109 records · Page 6Linked to original sources
PubMed1981

Relations between iron and vanadium metabolism: in vivo incorporation of vanadium into iron proteins of the rat.

In vivo experiments with 48V and 59Fe radiotracers were performed to study the association of V with Fe proteins. Each male rat was injected ip with 10 micrograms 48VO2+ and then with 1 microgram 59Fe3+ to label Fe-containing proteins. The radioactivities incorporated were measured in plasma transferrin, red blood cell hemoglobin, liver ferritin, partially purified heart myoglobin, and liver mitochondrial and microsomal cytochromes b and c and ferriporphyrin. Liver ferritin can bind V in vivo similarly to plasma transferrin, as shown by gel filtration and immunoprecipitation. Negligible amounts of 48 V were incorporated into hemoglobin, partially purified myoglobin, and cytochromes b and c. These findings suggest that the nonenzymatic Fe-containing proteins may be involved in the V metabolism.

Animals↗
PubMed1986

Vanadium metabolism in sheep. III. Influence of dietary vanadium on kinetics of 48V administered orally or intravenously and comparison of compartmental and graphical models.

Radiotracer techniques were used to investigate the influence of dietary stable V on the excretion, distribution and blood clearance kinetics of 48V in 14 rams averaging 58 kg body weight. Rams were fed a basal diet with added levels of 0, 50 or 200 mg/kg V as NH4 VO3 for 25 wk before either oral or iv administration of the isotope. A three-compartment model was determined by graphical logarithmic analysis of blood disappearance data from iv-dosed rams and compared with a simultaneous multicompartment model, which made it possible to ascribe physiological processes to the components of the graphical model. The principal route of excretion of 48V administered iv was via urine, whereas the isotope given orally was excreted almost entirely by way of feces, resulting in low tissue and urinary 48V levels. Increasing dietary V increased (P less than .05) the percentage of dose excreted in urine regardless of dosing route, but dietary V had no effect on 48V excreted in feces. Stable dietary V had no effect on blood clearance rates of orally or iv-dosed rams. Dietary V addition decreased 48V concentration in kidney (P less than .01), liver, spleen, testes and muscle (P less than .05) of iv-dosed rams, but had no effect in rams dosed orally. Kidney, bone, liver and spleen retained the highest levels of 48V activity 144 h after dosing. Dietary V appeared to have a minimal effect on V kinetics in rams.

Administration, Oral↗
PubMed1994

Evidence of multiple metabolic routes in vanadium's effects on layers. Ascorbic acid differential effects on prepeak egg production parameters following prolonged vanadium feeding.

The development of V toxicity was followed over a 28-d period in 25-wk-old Leghorn layers fed 20 mg ammonium metavanadate/kg diet (Days 1 to 14) followed by 30 mg/kg diet (Days 15 to 28). Then, over a second 28-d period, the responses to V and supplemental ascorbic acid (AA) fed at 500 or 1,000 mg/kg diet (Days 29 to 42) followed by 1,500 or 3,000 mg/kg diet (Days 43 to 56) were examined. Feed consumption, egg weight, Haugh units (HU), and BW measurements indicated that the response to V was multifactorial, but of differing intensities and time-frames for the variables. Haugh units were lowered rapidly (3 d, P < .05) in response to V feeding, but HU values decreased only slightly when dietary V was increased to 30 mg/kg. In contrast, egg production was decreased moderately by 20 mg V/kg and a considerable further reduction in egg production resulted from increasing the V to 30 mg/kg. Ascorbic acid supplementation differentially affected these responses: BW, egg production, and egg weight were improved significantly in the V-fed group receiving an AA supplement, as compared with those fed V only. Haugh unit values, however, were not improved by AA supplementation in groups receiving V. Foam functional properties, which also were changed by V feeding, were not corrected by AA feeding. The results suggest that the toxic effects of V are mediated through more than one physiological mechanism. One mechanism, which includes negative effects on BW, egg production, and egg weight, is responsive to the additional reducing equivalents provided by supplemental AA. Another mechanism, which is apparent from the effect of V on egg HU values, is not ameliorated by AA supplementation after toxicity developed.

Animals↗