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J. Braz. Chem. Soc. vol.25 no.6 São Paulo June 2014.

Since Martin Henze discovered in 1911 that ascidians accumulate high vanadium concentrations (up to 105 to 106 times higher than the values found in sea water), the interest in investigating the function of this metal in hyper-accumulator organisms has been increased.6 However, no-one has been able to determine the function of this element in these organisms. After the Henze discovery some other vanadium hyper-accumulator species of marine organisms were found including holothurians.

Recently, some polychaeta species were discovered as vanadium hyper-accumulators8,9 and the accumulation mechanism was similar to that found in ascidians despite phylogenetic distance between these organisms.10 This fact has brought attention to the discussion about the role of this metal. Many data are found in the literature about the function of this metal in hyper-accumulator organisms (as an oxygen carrier, energy source, anti-microbial defense and anti-predation), but none of these hypotheses have been confirmed.

Regarding the mechanism of vanadium speciation in biomolecules of marine organisms, the only known protein was isolated from ascidians and named vanabin.

The vanabin family consists of at least five small proteins: vanabin 1 through 4 and vanabin P, which are composed of approximately 90 amino acids including 18 cysteine residues. Recombination of vanabin 1, P and 2 were found to bind up to 20 vanadium ions in the +4 oxidation state (V+4) with dissociation constant of ca. 2 × 10-5 mol L-1.14 This biomolecule group has a molecular weight ranging from 10.46 to 28.03 Da.

Michibata et al.elucidated the incorporating process of V+5 present in seawater by ascidians. The V+5 is incorporated into vanadocytes, where V is bound to vanabin and reduced to +4 oxidative state with NADPH produced by the pentose-phosphate route. The V+4 bound with vanabin is transferred to an unknown protein to the vacuolar membrane, where it is trapped with metal-binding domains of a metal ATPase on the vacuolar membrane surface and is stored into vanadocytes vacuoles having both high levels of H+ and SO42–. The V+4 is further reduced to V+3 by an unknown reducing agent, whose oxidative state predominates in vanadocytes in a proportion of 97.6 (V+3):2.4(V+4).

In this my monograph (see. In RG) there are data (the literature): 

Book: П.Ф. Забродский, В.Г.Мандыч. Иммунотоксикология ксенобиотиков. Саратов, СВИБХБ. 2007. 420 p. P.F. Zabrodskii, V.G.Mandych. Immunotoxicology of xenobiotics. Saratov, Saratov Military Institute of Biological and Chemical Safety, 2007. 420 p.

П.Ф.Забродский, В.Г.Мандыч, P.F.Zabrodskii, V.G.Mandich

[Show abstract]

Saratov , Saratov Military Institute of Biological and Chemical Safety edited by P.F.Zabrodskii, 01/2007; Saratov Military Institute of Biological and Chemical Safety., ISBN: 978-5-91272-254-7

Literature data , unfortunately, are not new .

 P.F. Zabrodskii, V.G.Mandych. Immunotoxicology of xenobiotics. Saratov, Saratov Military Institute of Biological and Chemical Safety, 2007. 420 p.

  П.Ф. Забродский, В.Г.Мандыч. Иммунотоксикология ксенобиотиков. Саратов, СВИБХБ. 2007. 420 p. 

9.3 . Vanadium

Vanadium is contained in the body mainly in soft tissue (about 18 mg). Daily intake of vanadium is 2 mg . Vanadium is used in various alloys used in aircraft , missile , automotive, textile and paint industry , in the production of glass and glazes .

The first report on the role of vanadium as an essential element , appeared in 1971. Vanadium is involved in redox reactions in the cell membranes . Vanadium compounds have long been used as a stimulant in cases of anemia , for the treatment of syphilis , tuberculosis , neurasthenia, rheumatism [ Zabrodskii PF , 1998; Venugopal B., Luckey T.D., 1978 ] .

Vanadium poisoning can occur in a production environment or under excessive receiving chemotherapeutic agents , eat foods rich in this element.

Vanadium toxicity is low, the cumulative effect is absent. Mechanisms of toxic effects are associated with inhibition of 13 enzyme systems [ Zabrodskii PF , 1998] , in violation of lipid metabolism, reduction in the synthesis of phospholipids, cholesterol. Vanadium compounds like insulin catalyze the oxidation of glucose. Like vanadium arsenate replacing the phosphate by reaction with glyceraldehyde -3- phosphate and breaking phosphorylation , ATP synthesis , inhibits various ATPase . The toxicity of vanadium is reduced by ascorbic acid [ Ershov YA, Pletnev TV 1989 ] .

Chronic poisoning Vanadium can cause respiratory tract irritation , bronchitis and pneumonia [ Zabrodskii PF, 1998].

Vanadium reduces phagocytic activity of macrophages in rabbits at a concentration of 5 and 10 ug / ml in vivo at 20 h exposure , respectively 45 and 85 % [Waters MP et al., 1974 ] . A similar reaction indicated by granulocytes in rat entering the body of water in a concentration of ammonium metavanadate was 0.15 mg / ml [Zaporowska H., Wasilewski W., 1992 ] . A reduction in lymphocyte blast transformation under the influence of vanadium [Shifrine M., et al., 1984 ] . In mice, a trace amount of vanadium chloride inhibited the development of DTH reaction to nitrilhlorid without changing the level of the humoral immune response [Hoshishima K. et al., 1985 ] .

Bronchial asthma vanadium compounds under the action accompanied by an increase in the blood concentration of IgE and IgG [Koller LD, 1984 ] .

Thus , vanadium lowers indicators of innate immunity and cellular immune response.