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A functional role for vanadium in higher animals and humans has not yet been identified. Vanadium mimics insulin and stimulates cell proliferation and differentiation. Vanadium inhibits various ATPases, phosphatases, and phosphoryl-transfer enzymes. The response of thyroid peroxidase to changing dietary iodine concentrations has been shown to be altered in vanadium-deprived rats. Vanadium-deprived goats show elevated abortion rates and decreased milk production. In vitro, vanadium in the form of vanadate regulates hormone, glucose, and lipid metabolism; however, vanadium most probably exists in the vanadyl form in vivo.

Physiological role

The absorption of ingested vanadium is less than 5%, and therefore most ingested vanadium is found in the feces. Absorbed vanadate is converted to the vanadyl cation, which can complex with ferritin and transferrin in plasma and body fluids. Highest concentrations of vanadium are found in the liver, kidney, and bone. However, very little of the absorbed vanadium is retained in the body. Patterson and coworkers, in 1986, investigated vanadium metabolism in sheep and suggested a compartmental model with certain tissues constituting a “slow turnover” pool where the turnover times for vanadium might exceed 400 days. Other tissues were suggested to constitute a “fast turnover” pool with vanadium residency of about 100 hours.


Vanadium is an essential component of different enzymes, Nitrogen-fixation bacteria, cyanobacteria and especially in ascidians but the structure of Vanadium-dependent enzymes is not fully known and reasons for Vanadium essentiality for organisms are yet to be explored.

Food sources

Foods rich in vanadium include mushrooms, shellfish, black pepper, parsley, dill seed, and certain prepared foods. Myron and coworkers, in 1977, reported that processed foods contained more vanadium than nonprocessed foods. Byrne and Kosta, in 1978, also suggested that beer and wine may contribute an appreciable amount of vanadium to the diet. Commodity groups highest in vanadium are grains and grain products, sweeteners, and infant cereals. Analysis of data from the 1984 Food and Drug Administration Total Diet Study (Pennington and Jones, 1987) showed grains and grain products contributed 13-30% of the vanadium in adult diets. Beverages were also an important source for adults and elderly men (26-57%). This study also reported that 88 percent of the foods consumed had concentrations less than 2 μg/100 g. Canned apple juice and cereals were the major contributors of vanadium to the diets of infants and toddlers.

Recommended daily allowance

Pennington and Jones, in 1987, reported that vanadium intake ranged from 6.5-11 μg/day for infants, children, and adolescents. The intake of vanadium for adults and the elderly ranged from 6-18 μg/day.


A deficiency of vanadium results in increased abortion rates. A biological role of vanadium in humans has not yet been identified.


There is no evidence of adverse effects associated with vanadium intake from food, which is the major source of exposure to vanadium for the general population. Most vanadium toxicity reports involve industrial exposure to high levels of airborne vanadium. The most toxic vanadium compound is vanadium pentoxide, but because vanadium pentoxide is not a normal constituent of food, supplements, or drinking water. The overdoses of vanadium causes desquamative enteritis, mild liver congestion with fatty changes, and slight parenchymal degeneration of the renal convoluted tubules.

There is human evidence of mild gastrointestinal effects (abdominal cramps, loose stool) primarily in patients with diabetes and animal evidence of more severe gastrointestinal effects (diarrhea, death) after ingestion of vanadium compounds.

Vanadium compounds may cause anemia and changes in the leukocyte system. Animal studies of hemolytic activity of vanadium salts have conflicting results. Fawcett and coworkers, in 1997, showed no effects of oral vanadyl sulfate (0.5 mg/kg body weight/day) on hematological indexes, blood viscosity, and biochemistry in a 12-week, double-blind, placebo-controlled trial in 31 athletes.

Exposure to vanadate induced an increase in blood pressure and heart rate in rats. Boscolo and coworkers, in 1994, showed an increase in arterial blood pressure following chronic exposure of rats to 1, 10, and 40 μg/mL of vanadium for 6 or 7 months. These changes were not dose-dependent.

No evidence of reproductive abnormalities after ingestion in humans was found. Two animal studies evaluating the reproductive toxicity of vanadium have been reported: in one, Llobet and coworkers, in 1993, observed that at 60 and 80 mg/kg body weight/day, a significant decrease in pregnancy rate occurred; in the other, Domingo and coworkers (1986) found no effects on fertility or reproduction in rats gavaged up to 20 mg/kg body weight/day with sodium metavanadate.

Vanadium intake in humans may also include green tongue, fatigue, lethargy, and focal neurological lesions.

Medicinal Role

In laboratory animals, vanadium mimics insulin (diminishes hyperglycemia and improves insulin secretion) and inhibits the activity of various enzymes.


Anke M., 1986, “Arsenic. In: Mertz W, editor. , ed. Trace Elements in Human and Animal Nutrition , Vol. 2, 5th ed.,” Orlando, FL: Academic Press. P. 347–372.

Boden G., et al., 1996, “Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus,” Metabolism; 45:1130–1135. [Web Reference]

Byrne A.R. and Kosta L., 1978, “Vanadium in foods and in human body fluids and tissues,” Science of the Total Environment; 10(1): 17-30. [Web Reference]

Goldfine A.B., et al., 1995, “In vivo and in vitro studies of vanadate in human and rodent diabetes mellitus,” Molec Cell Biochem; 153:217–231. [Web Reference]

Heyliger C.E., Tahiliani A.G. and McNeill J.H., 1985, “Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats,” Science; 227:1474–1477. [Web Reference]

Imtiaz M., et al., 2015, “Vanadium, recent advancements and research prospects: a review,” Environment International; 80: 79-88. [Web Reference]

Institute of Medicine (US) Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington (DC): National Academies Press (US); 2001. 13, Arsenic, Boron, Nickel, Silicon, and Vanadium. [Web Reference]

Myron D.R., Givand S.H. and Nielsen F.H., 1977, “Vanadium content of selected foods as determined by flameless atomic absorption spectroscopy,” J. Agric Food Chem; 25:297–300. [Web Reference]

Nielsen, Forrest H., and Eric O. Uthus. "The essentiality and metabolism of vanadium." Vanadium in biological systems. Springer Netherlands, 1990. 51-62. [Web Reference]

Pennington J.A. and Jones J.W., 1987, “Molybdenum, nickel, cobalt, vanadium, and strontium in total diets,” J. Am Diet Assoc; 87:1644–1650. [Web Reference]

Soetan K.O., Olaiya C. O. and Oyewole O.E., 2010, “The importance of mineral elements for humans, domestic animals and plants-A review,” African Journal of Food Science; 4(5): 200-222. [Web Reference]

Wei CI, Al Bayati MA, Culbertson MR, Rosenblatt LS, Hansen LD. 1982. Acute toxicity of ammonium metavanadate in mice. J. Toxicol Environ Health 10:673–687. [Web Reference]

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