Vanadium excretion

Dimond EG, Caravaca J, Benchimol A. 1963. Vanadium Excretion, toxicity, lipid effect in man. Am J Clin Nutr 12 49-53. 

Vanadium, a metal, has many applications in the steel, automotive, and chemical industries. It constitutes a significant portion of exhaust from fuels. Cleaners of oil-fired power plant burners have high urinary vanadium excretion (Maroni et al. 1987). A description of Australian boiler cleaners included trembling, headache, blindness, nervous troubles, and psychic derangement (Thomas and Stiebris 1956). The earliest reports of vanadiumism in the twentieth century described symptoms of hysteria and melancholia accompanied by tremor, vertigo, headache, neuroretinitis, and amaurosis (Dutton 1911). 

Hansard SL, Ammeeman CB and Henry PR (1982b) Vanadium metabolism in sheep. II. Effect of dietary vanadium on performance, vanadium excretion and bone deposition in sheep. J Anim Sci 55 350-356. 

Absorbed vanadium is primarily excreted in the urine, and it was detectable in 12 of the workers for periods of up to 2 weeks. Urinary vanadium concentrations were elevated in workers exposed to mean air concentrations of 0.1-0.28mg/m but there was no correlation between the air and urinary concentrations. Although most absorbed vanadium was excreted within 1 day after cessation of exposure, increased excretion relative to unexposed controls continued for more than 2 weeks among chronically exposed workers. ... 

Kent NL, McCance RA. 1941. The absorption and excretion of minor elements by man. I. Silver, gold, lithium, boron and vanadium. Biochemical Journal 35 837-844. 

To date, there is limited published material concerning the pharmacokinetics of vanadium compounds in humans. The concentration of vanadium in humans not dosed with the metal is extremely low and at the limits of detection of many of the analytical techniques used. It is not possible to ascertain if the large differences observed in different populations are the result of environmental exposure or experimental variability. Studies using blood have shown vanadium levels of 0.4 to 2.8 pg/L in normal people. The serum contains the largest amount of vanadium with concentration values ranging from 2 to 4 pg/L using atomic absorption spectroscopy [90], The upper limit of vanadium in the urine of normal people was reported to be 22 pg/L, with excretion values averaging below 8 pg/24 h. Vanadium is widely available in nutrition stores for athletes, who believe it to be a nonsteroidal compound that increases muscle mass at a dose of approximately 7 to 10 mg day, without any reports of toxicity [91]. 

In humans, 0.1-1% of orally administered vanadium is absorbed through the gut. Lung and gut absorption increases with the solubility of the vanadium compound. Vanadium pentoxide is 100% absorbed by inhalation. Vanadium is not absorbed through the skin. When absorbed, 60% of the vanadium is excreted by the kidneys within 24 h of administration. Vanadium can pass through the blood-brain barrier. 

No studies were located regarding excretion in humans after oral exposure to vanadium. 

Since vanadium is poorly absorbed in the gastrointestinal tract, a large percentage of vanadium is excreted unabsorbed in the feces in rats following oral exposure. More than 80% of the administered dose of ammonium metavanadate accumulated in the feces after 6 days (Patterson et al. 1986). After 2 weeks of exposure, 59.1 18.8% of sodium metavanadate was found in the feces (Bogden et al. 1982). However, the principal route of excretion of the small absorbed portion of vanadium is through the kidney in animals. 

Enhanced excretion of vanadium was achieved with chelation therapy provided by deferoxamine mesylate (DFOA) (Gomez et al. 1988). Humans or animals with vanadium poisoning have not been helped by the chelating agent dimercaprol (BAL), which is often effective in lessening the toxicity of other metals (Lusky et al. 1949). Intraperitoneal injections of ascorbic acid and of ethylene diamine tetraacetate (EDTA) reduced vanadium-induced morbidity in mice and rats (Jones and Basinger 1983 Mitchell and Floyd 1954). 

Domingo JL, Llobet JM, Tomas JM, et al. 1986. Influence of chelating agents on the toxicity, distribution, and excretion of vanadium in mice. J AppI Toxicol 6 337-341. 

The (metabolic) pathways of dietary vanadium, such as vanadate [H2V04], can be expressed as illustrated in Scheme 5.1 after oral uptake, vanadate reaches the gastrointestinal tract, where it is partially reduced and precipitated to vanadyl (VO ) hydroxides, which are excreted with the faeces. Another portion is absorbed and circulated in the blood, where it undergoes redox speciation and complexation by the serum proteins transferrin and albumin. Vanadate and vanadyl are finally incorporated into cells, mainly those of the liver, spleen and kidney. Excretion is achieved via the urine. Part of the vanadium is taken up by bones, where the mean retention time is comparatively long. 

In general, these results are in agreement with distribution studies, using V-labelled BMOV (7a in Figure 5.2) and vanadyl sulfate.P l The isotope is a jS+ and y emitter, and decays with = 16 days to Ti. In particular, these studies showed that BMOV is more effectively distributed towards the tissues (and less effectively secreted) than vanadyl sulfate over a period of 24 h, both when applied orally and intraperitoneally to rats. The highest concentrations were found in bone, followed by kidney and liver. The residence time in bone is 11 days for vanadium delivered in the form of vanadyl sulfate, and 31 days for BMOV. The amount of V excreted in the faeces 24 h after oral gavage were estimated to be 75% for vanadyl sulfate and 62% for BMOV. On the basis of other studies, absorption of orally administered vanadium is much lower and comes close to 1 % in the case of vanadyl sulfate. 

Thus, the different absorption rates, the effects of other dietary components on the forms of vanadium in the stomach, and the rate of transformation into V appear markedly to affect the proportion of ingested vanadium that is absorbed (Patterson et al. 1986, Chasteen et al. 1986, Wiegman et al. 1982, Hansard etal. 1982b). Studies with humans and an intake of 11 to 39 pg V per day showed renal and lactational excretions of vanadium of approximately 5% and 16%, respectively. The apparent absorption rate varied between 10 and 25% (Table 27.5) (Anke et al. 1998d). Besides the form of vanadium, it is also the quantity of vanadium present that influences the absorption rate of this ultratrace element. 

Fecal excretion of the nutritional vanadium intake amounts to 96% in both sexes, and to 79% in lactating tvomen (Tables 27.5 and 27.6). Most of the ingested vanadium is not absorbed, and the form of the diet (mixed or ovo-lacto-vegetarian) has no effect on the fecal excretion rate (see Table 27.5). On average, adults of both sexes and with either form of diet eliminate 4% of the nutritional vanadium intake renally (range 2-6%). 

Titanium has a tendency to accumulate in tissues. The concentrations can be very high, as indicated in Table 9.5. Titanium was not excreted in the urine of hamsters injected with metal salts (Merritt et al, 1992). Small concentrations were found in the serum, red blood cells and organs. Only 5.5% of the injected titanium was found in the kidneys, liver, lung and spleen tissues. The authors suggest that titanium accumulates at the injection site due to the high stability of the titanium dioxide that is formed at physiological conditions. In the same study nearly all the injected vanadium was recovered in the urine. This behaviour is similar to that of nickel and cobalt, and is related to the formation of highly soluble compounds. 

Vanadium can be absorbed through the respiratory and gastrointestinal tracts, although the gastrointestinal route is the most studied. Vanadium occurs in the diet, or as a pharmacological agent, mainly as vanadyl or vanadate. Vanadate is transformed into vanadyl in the stomach [67], which primarily is the absorbed form. Most studies indicate that relatively little (<5%) ingested vanadium is absorbed and the remainder is excreted in the feces [68-74]. However, as with all substances, other dietary components probably affect absorption. The main route of excretion of absorbed vanadium is in the urine with lesser amounts lost in the feces, probably via the bile [74-77]. 

In the human gastrointestinal tract, only 0.1-1% of vanadium contained in the diet is resorbed. For some laboratory animals, however, fairly high resorption of vanadium from the diet with a predominance of casein and carbohydrates has been observed. Vanadium resorbed in the form of metavanadate ions (VOj") containing V is reduced by glutathione in the blood to VO + ions that contain V and form 2 1 metal-protein complexes with ferritin and transferrin. Transferrin then obviously provides the distribution of vanadium in the tissues. Vanadium is also present in a metallopro-tein (metaUoporphyrin) called haemovanadin. Excessive intake of vanadium is excreted in the urine. 

Later, Chasteen, Lord, and Thompson used EPR to determine the chemical forms of both absorbed vanadium in tissue and excreted vanadium in the urine and feces of rats given VOSO4 in drinking water over long periods. EPR signals were well defined in the stomach, duodenum, liver, spleen, kidney, lung, and elimination products [78],... 

Vanadium salts are not readily absorbed in the intestine. They are mainly excreted in the urine and to a lesser degree in the stool. Even when highly soluble... 

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