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OCR for page 534
Vanadium
Vanadium (V), a bright white metal in the pure state, was named for
Vanadis, the Norse goddess of beauty, in 1830 (Busch, 19611. Under-
wood (1962) noted that vanadium has been considered a rare element
because there are few commercially workable deposits; however, it is
actually one of the more prevalent trace elements. The element is found
in some 50 different naturally occurring minerals, among which car-
notite, roscoelite, vanadinite, and patronite are the most important
industrial sources (Faulkner-Hudson, 1964~.
Vanadium usually occurs in the earths crust as relatively insoluble
salts and is present in some sediments as oxovanadium (IV) anion
bound to organic chelates (Yen, 1972~. Tool and cutting steel, high-
strength structural steel, and wear-resistant cast iron often contain 0.1
to 0.5 percent vanadium. There are several reviews on vanadium (Cur-
ran and Burch, 1967, Lillie, 1970; National Research Council' 19741.
ESSENTIALITY
Hopkins and Mohr (1974) provide evidence that vanadium meets all
criteria for essentiality. Schwarz and Milne (1971a,b) reported that
vanadium was necessary for growth of rats raised in a trace element-
controlled, all-plastic isolator. The addition of sodium orthovanadate
(Na3VO4) to rat diets enhanced growth with 0.1 ppm vanadium opti-
mizing performance. This growth response was confirmed by Strasia
534
OCR for page 535
Vanadium
535
(1971~. Hopkins and Mohr (1971b) noted retarded feather growth in
chicks consuming a diet containing less than 10 ppb vanadium. In
calves, the addition of 0.1 mg sodium metavanadate per kilogram of
body weight for 4 months increased growth by 11.5 percent, as well as
increasing erythrocyte number 5.5 percent and blood hemoglobin
content 7.1 percent (Drebickas, 1966~. Nielsen and Ollerich (1973)
observed increased hematocrit values, increased epiphyseal plate, and
decreased primary spongiosa in the tibia of vanadium-deficient chicks
receiving 3~35 ppb of the element.
Hopkins and Mohr (1974) reviewed the vanadium literature and
reported that reproductive efficiency is impaired by a deficiency of the
mineral. Vanadium's effect in reducing dental caries is still not resolved
(Hadjimarkos, 19661.
Vanadium increased oxidation of phospholipids by washed liver
suspensions in vitro (Bernheim and Bernheim, 19381. Curran (1954)
discovered vanadium's ability to inhibit cholesterol biosynthesis for a
microbial squalene synthetase system. Several later reports indicate
altered blood lipid levels during vanadium deficiency (Hopkins and
Mohr, 1971a, 1974; Nielsen and Ollerich, 19731. Recent reports
(Nielsen and Myron, 1976; Nielsen and Uthus, 1977) suggest that vana-
dium has a role in labile methyl metabolism in the chick.
METABOLISM
Metabolism of vanadium has been discussed in several reviews (Scott
et al., 1951; Soremark and Ullberg, 1962; Hopkins and TiltoIl, 1966~.
Radioactive tracer studies by Comar and Chevallier (1967) have shown
that vanadium is not readily absorbed from the digestive tract of the rat;
however, the average body concentration was proportional to dietary
intake. Faulkner-Hudson (1964), citing a report by Scott et al. (1951),
indicated that only 0.5 percent of the radiovanadium administered
intragastncally to rats was absorbed. Less that 1 percent vanadium was
absorbed following ingestion in man (Curran et al., 1959) and in sheep
(Hansard, 1975~.
Excretion of the injected or absorbed metal is mainly by the kidneys.
Talvitie and Wagner (1954) noted that vanadium, as sodium metavana-
date injected intravenously, was excreted rapidly by the kidneys with
60 percent of the dose appearing in the urine within 24 hours in rats
and rabbits. Sixty-six percent of vanadium as VOCI2 injected intra-
muscularly in rats was eliminated in urine within 24 hours (Pepin et al.,
19771. Similar values were observed (Hopkins and Tilton, 1966) when
OCR for page 536
536 MINERAL TOLERANCE OF DOMESTIC ANIMALS
approximately 45 percent of the injected isotope (48VOCI2+) was lost in
urine and 9 percent in the feces of rats. Relatively high retention of
48V in bones and kidneys of chicks following oral administration of
vanady! dichloride was observed (Hathcock et al., 1964~. Radioisotope
distribution studies (Hathcock e' al., 1964; Comar and Chevallier,
1967; Hansard, 1975) indicate that the element is retained princi-
pally by kidney and also by bone, liver, and spleen, although clear-
ance from blood Hopkins and Tilton, 1966) and soft tissues (Thomas-
sen and Leicester, 1964) is rapid. Growing bone (Hathcock et al., 1964;
Parker and Sharma, 1978) and possibly kidney and major organs retain
the metal to a small degree. Radioactive 45V2O5 was concentrated in
bones and teeth of mice and rats 7 days after injection (Soremark et al.,
..
1962; Soremark and Ullberg, 1962~. Other tissues also retained the
isotope; the decreasing order of the radioactivity was visceral yolk sac,
epitheliums, lactating mammary gland, renal cortex, liver, lung, skin,
and salivary gland. Vanadium appears to exist in tissues in a protein-
bound form (Johnson et al., 19741. Vanadate taken up by the red
blood cell is reduced to the +4 oxidation state in the cytoplasm (CantIey
and Aisen, l979~. Oxidation state does not appear to affect metabolism
of vanadium (Sabbioni et al., 1978~.
SOURCES
Vanadium is distributed widely in nature, occurring in many plants and
animals (Curran and Burch, 1967; Underwood, 19771. The level in the
earth's crust has been estimated at 110 (Goldschmidt, 1958) to 150 ppm
Winogradov, 1959~. Of special concern is the vanadium content of rock
phosphates, which may be used as phosphorus sources for animal diets.
Vanadium concentration, although varying with location, may be as
high as 6,000 ppm in some rock phosphate deposits (Romoser et al.,
1960~. Berg (1963) reported that a commercial tricalcium phosphate
contained 0.25 percent vanadium pentoxide (1,400 ppm V) and reduced
growth in poultry receiving 1~20 ppm vanadium. Grazing animals are
exposed to elevated levels of many minerals due to ingestion of soil
(Healy, 1973; Thornton, 1974~. Most feed sources analyzed by Mitchell
(1957) contained less than 0.15 ppm on a dry weight basis. Analysis of
animal specimens, vegetables, and fruits (Soremark, 1967) indicated
that all samples contained less than 0.5 ppm vanadium (wet weight).
In the natural state, vanadium occurs with positive valences of two,
three, four, and five. The pentavalent salts are vanadates and the
quadrivalent ion forms vanadites (Faulkner-Hudson, 1964~. The most
OCR for page 537
Vanadian
537
important compound in industry is the pentoxide (V2Os) (Fairhall,
1949~. The bioavailability of venous forms of vanadium has been in-
vestigated by Schwarz and Milne (l97lb). In their studies with mice,
sodium orthovanadate was more effective in promoting growth than
sodium metavanadate, while the pyrovanadate salt had no activity.
TOXICOSIS
Numerous reviews on vanadium toxicity are available (Sjoberg, 1950;
Stokinger, 1955, 1963; Faulkner-Hudson, 1964; Lillie, 1970; National
Research Council, 1974~. Vanadium appears to exert its toxic effect
through inhibition of enzymes (Underwood, 1977) and cell damage from
lysis (Waters et al., 19751. Vanadate has been found to inhibit (Na,
K)-ATPase (CantIey et al., 1977, 1978; Nechay and Saunders, 1978;
Goodno, 1979; Nieder et al., 1979) and activate cardiac adenylate
cyclase (Grupp et al., 1979~.
LOW LEVELS
Industrial exposure to vanadium, through breathing of airborne particu-
late matter, was found to cause irritation of the nose and throat, ano-
rexia, nausea, and diarrhea in workers (Fairhall, 19491. Toxicosis in
humans from ingestion is uncommon except as incidental to high aerial
concentrations (National Research Council, 19741. The chick appears
to be most susceptible to orally induced vanadium toxicosis (Table 39),
consequently the bird is the most studied model for toxicity. Animals
that have been shown to adapt to high vanadium levels include the rat
(Daniel and Lillie, 1938; Strasia, 1971) and chick (Williams, 19731.
Studies suggest that alterations in rumen function can result from
ingestion of vanadium. In vitro dry matter digestibility was reduced in
rumen fluid inoculum from lambs by 7 ppm vanadium added as sodium
ortho- or metavanadate (Williams, 1973~. Martinez and Church (1970)
reported reduced in vitro cellulose digestion by washed suspensions of
rumen microorganisms with 5 ppm vanadium as sodium metavanadate.
These results were in general agreement with studies by Jha (1966~.
Lillie (1970), citing a report by Heege (1964), noted cows exposed to
vanadium from fi~el oil soot on grazing areas showed weakness and
ataxia. Vanadium content of liver tissue ranged from 1.5 to 4.7 ppm
(wet weight).
Romoser et al. (1961) observed that chicks tolerated up to 20 ppm
vanadium in a corn-soybean meal diet, while Nelson et al. (1962) re-
OCR for page 538
538 MINERAL TOLERANCE OF DOMESTIC ANIMALS
ported that 35 ppm vanadium was toxic for chick growth. Hathcock e'
al. (1964) reported that 25 ppm vanadium as ammonium metavanadate
(NH4VO3) depressed growth and increased mortality, but 10 ppm vana-
dium had no effect. Berg (1963) found that two commercial samples of
tricalcium phosphate depressed chick growth when compared to other
phosphorus sources. The samples contained 0.25 percent vanadium
pentoxide (V2O5) contributing 28 ppm vanadium to the complete diet.
Berg et al. (1963) also found that 60 ppm vanadium as ammonium
metavanadate reduced hatchability of fertile eggs by 10 percent. Egg
production was depressed with 30 ppm vanadium, but only 15 to 20 ppm
were required to lower egg albumin quality. Other studies with poultry
are shown in Table 39.
Since experimental results with domestic animals are limited, labora-
tory animal studies may supplement available information. Vanadium,
as sodium metavanadate (NaVO3) was slightly toxic to rats at 25 ppm
and distinctly toxic at 50 ppm (Franke and Moxon, 1937~. Daniel and
Lillie (1938) observed no effect in rats receiving 11.5 and 22 ppm vana-
dium as sodium metavanadate over 12 weeks, but 92 ppm was very
toxic and 368 ppm was lethal within 10 weeks. MuhIer (1957) reported
reduced growth and higher mortality in rats receiving 20 ppm vanadium
as vanadium pentoxide (V2O5) in drinking water. At 40 ppm, a 100
percent death rate was observed within 65 clays. Schroeder and Balassa
(1967) gave mice 5 ppm vanadium as vanadyl sulfate (VOSO4) in dnok-
ing water from weaning until natural death and found no toxicosis in
terms of growth, survival, or life span, but the metal accumulated in the
heart and spleen. A similar long-term study with rats receiving 5 ppm
vanadium showed no accumulative toxicity (Schroeder e! al., 19701.
HIGH LEVELS
Few acute vanadium toxicity studies are available. Platonow and
Abbey (1968) studied the toxicosis of vanadium in calves. Gelatin cap-
sules of ammonium metavanadate, given orally at daily dosage levels of
1, 3, 5, 7.5, 10, 15, and 20 mg vanadium per kilogram of body weight,
produced intoxication at the three higher levels. The dose of 20 mg
resulted in adverse effects within 3 days, including diarrhea, dehydra-
tion, emaciation, and prostration. Gross pathological changes were
congestion of liver and lungs, diffuse hemorrhage covering the kidneys
and heart, ruminal ulcers, and hemorrhagic inflammation of the in-
testinal tract. The greatest concentration of vanadium was found in
kidney, liver, and spleen.
Hansard (1975) observed a 65 percent death loss within 80 hours in
OCR for page 539
Vanadium
539
sheep given 40 mg vanadium per kilogram of body weight as ammonium
metavanadate. Vanadium content of kidney, liver, bone, spleen, lung,
and muscle was elevated by treatment. Histological examination
showed evidence of liver degeneration and nephritis. Hansard et al.
(1978) also reported reduced growth and feed utilization and diarrhea in
sheep fed 400 ppm vanadium as ammonium metavanadate for 84 days
(Table 39~.
Romoser et al. (1960) apparently were the first to show that dietary
vanadium retarded the growth rate of chicks. When given as the cal-
cium salt [Ca3(V0412] the Peso for vanadium was between 300 and 350
ppm, but growth was inhibited at levels above 20 ppm.
Proescher et al. (1917) reported the ~0 in rats upon subcutaneous
injection was 20 to 30 mg vanadium per kilogram of body weight as
ammonium metavanadate. Necrosis of renal convoluted tubules, fatty
degeneration of the liver, adrenal hemorrhage, constriction of visceral
arteries, and inflammatory lesions in the intestinal tract were noted.
FACTORS INFLUENCING TOXICITY
Various compounds have been credited with alleviating vanadium
toxicity. Wright (1968) found that 2,000 ppm supplemental chromium
reduced the death rate in chicks from X6.6 to 13.3 percent when fed 20
ppm vanadium. This author suggested that chromium antagonizes
vanadium uncoupling of oxidative phosphorylation and retards the in-
testinal absorption of vanadium. DeMaster (1972) was not able to con-
firm the role of vanadium in uncoupling of oxidative phosphorylation.
Chicks fed 5 ppm vanadium as NH4VO3 were affected adversely when
also supplemented with 500 ppm chromium as Cr(C2H302) (Hunt and
Nielsen, l979~. Moxon and Rhian (1943) observed that rats given 11
ppm selenium in drinking water died more quickly when selenium was
in combination with 5 ppm vanadium.
Mitchell and Floyd (1954) and Berg and Lawrence (1971) tested
ascorbic acid and ethylenediaminetetraacetate (EDTA) as antidotes in
experimental vanadium poisoning in mice and rats. EDTA may function
by preventing vanadium absorption (Hathcock et al., 1964), when fed
at twice the molar concentration of vanadium.
Diet composition greatly affected the degree of toxicity of dietary
vanadium (Mountain et al., 1959; Hathcock et al., 1964). Berg (1966)
and Hill (1979) showed that increasing dietary protein levels gave linear
decreases in the mortality rate of chicks, but Hansard (1975) found no
difference in performance or tissue levels of rats when protein level was
increased from 20 to 30 percent with vanadium levels up to 40 ppm.
OCR for page 540
540 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Research with poultry (Hafez and Kratzer, 1976a) suggests that vana-
dium may have a greater adverse effect when fed in purified rather than
natural diets.
TISSUE LEVELS
Vanadium toxicosis has not been studied as extensively as many of the
other minerals, although the recent recognition of high concentrations
in some phosphates, coals, and petroleum products has increased in-
terest in the movement of the element from the environment to animals
and man.
In calves given lethal amounts of vanadium, none was detected in
skeletal muscle (detection limit, 0.01 ppm), but up to 5.1 ppm (wet
weight) was found in liver (Platonow and Abbey, 19681. It is apparent
that animal tissues increase in vanadium content in response to dietary
exposure (Comer and Chevallier, 1967; Hopkins and Mohr, 1971b).
Soremark (1967) reported that calf liver and muscle contain 10 ppb or
less, while milk values were generally lower than 100 ppb (wet weight).
Other studies (Hopkins and Tilton, 1966) have shown no particular
accumulation in adipose tissue.
In studies with rats (Parker and Sharma, 1978) receiving 50 ppm
vanadium as vanadyl sulfate or sodium orthovanadate in drinking water
for 90 days, tissue accumulation was greatest for kidney, followed by
bone, liver, and muscle. In general, tissue vanadium concentrations
were greater in animals receiving the sodium orthovanadate.
Hansard et al. (1978) fed 10, 100, and 200 ppm vanadium as am-
monium metavanadate to sheep for 84 days and found increased levels
of vanadium in bone, liver, kidney, and muscle with 200 ppm vanadium
(Table 40~. Kidney vanadium levels were also increased when 100 ppm
was fed.
MAXIMUM TOLERABLE LEVELS
The rat and chick appear to have a similar tolerance to vanadium, but
ruminants are less susceptible to toxicity. Reduced growth has been
obtained in day-old chicks with 8-10 ppm dietary vanadium as ammo-
nium metavanadate. Other studies with the young chick indicate a
tolerance of 25 ppm vanadium; a similar level fed to laying hens reduced
egg quality. Weanling rats tolerated 20 ppm vanadium as sodium meta-
vanadate but 40 ppm reduced growth. Growing lambs tolerated 200
OCR for page 541
Vanadium
541
ppm dietary vanadium as ammonium metavanadate with no effect on
growth rate but significant increases in tissue vanadium levels occurred
with this intake and also with 100 ppm vanadium in the diet. Lambs did
not consume feed containing 400 ppm vanadium. Suggested maximum
tolerable dietary levels for vanadium are 50 ppm for cattle and sheep
and 10 ppm for poultry. Research with poultry suggests that similar
levels of vanadium may have a greater adverse eject when fed in a
purified diet than when fed in a diet composed of natural ingredients.
SUMMARY
Vanadium has been shown to be essential for normal growth and proper
physiological function in all species studied. It has also been found to
be toxic in all animals studied. Vanadium appears to exert its toxic
effect through inhibition of enzymes and cell damage from lysis. Vana-
dium given daily at 20 mg/kg of body weight produced diarrhea, emacia-
tion, and prostration in calves within 3 days. Sheep showed a 65 percent
death rate within 80 hours when given 40 mg vanadium per kilogram
body weight as NH4VO3. Signs of toxicosis in calves and lambs include
diarrhea, depressed growth and performance, ataxia, and mortality.
EDTA appears to act as an antidote in vanadium toxicosis, possibly by
preventing absorption from the intestinal tract. The vanadium content
of most feedstuffs is generally low except in some rock phosphate
sources. Industrial contamination of air and water appears to be the
greatest source of vanadium to the environment.
OCR for page 542
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OCR for page 548
548 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TABLE 40 Effect of Dietary Vanadium on Tissue Vanadium of
Sheep
Tissue, ppm dry matter basis
Supplemental
Vanadium, ppm Bones Liver Kidney Muscle
O '0.19+0.03C 0.12+0.03C 0.23+0.04C 0,0400.00C
10 0.22 + 0 05C 0.18 + 0 04C 0.41 + 0.06C 0.05 + 0 01C
100 1.50 + 0 34c 0.96 + 0.12C 3.62 + 0.19~ 0.12 ~ ~ 01C
200 3.32 + O.23& 2.81 ~ 0.24& 1 1.13 + 0.46e 0.41 + 0.04&
a Means with standard errors. Means represent data from five sheep. Hansard et al., 1978.
bBone, ash weight basis.
C &,e Means in the same column with different superscripts are different (P < 0.05).
REFERENCES
Baker, D. H., and B. A. Molitoris. 1975. Lack of response to supplemental tin, vanadium,
chromium and nickel when added to a purified crystalline amino acid diet for chicks.
Poult. Sci. 54:925.
Berg, L. R. 1963. Evidence of vanadium toxicity resulting from the use of certain com-
mercial phosphorus supplements in chick rations. Poult. Sci. 42:766.
Berg, L. R. 1966. Effect of diet composition on vanadium toxicity for the chick. Poult.
Sci. 45:1346.
Berg, L. R., and W. W. Lawrence. 1971. Cottonseed meal, dehydrated grass and ascorbic
acid as dietary factors preventing toxicity of vanadium for the chick. Poult. Sci.
50: 1399.
Berg, L. R., G. E. Bearse, and L. H. Merrill. 1963. Vanadium toxicity in laying hens.
Poult. Sci. 42: 1407.
Bernheim, F., and M. L. C. Bernheim. 1938. Action of vanadium on tissue oxidations.
Science 88:481.
Bruffy, G. R., and R. P. Dowdy. 1979. Effect of dietary vanadium on cholesterol metab-
olism in guinea pigs Fed. Proc. 38:450. (Abstr.)
Busch, P. M. 1961. Vanadium: A Materials Survey. Bureau of Mines. I. C. 8060. U.S.
Department of the Interior, Washington, D.C.
Cantley, L. C., Jr., and P. Aisen. 1979. The fate of cytoplasmic vanadium, implications
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Representative terms from entire chapter:
dietary vanadium
