Disease relevance of Ammonium monovanadate

• Vanadium, as ammonium monovanadate, has been found to stimulate tumour cell proliferation in mice bearing a transplantable ascitic lymphoma [1].
• Treatment with 20 mg/kg 1,2-DMH for 6 weeks resulted in the formation of aberrant crypt foci (ACF), a putative preneoplastic lesion associated with colon cancer development, while cotreatment with ammonium monovanadate (0.5 ppm in the drinking water) reduced ACF formation by 50% (P < 0.001) [2].
• 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) [3].
• Inclusion of 28.5 ppm V as ammonium vanadate also reduced egg production and feed consumption but had no significant effect on egg weight or change in body weight during the 4-week test period [4].

High impact information on Ammonium monovanadate

• Ammonium vanadate (10 microM) blocked differentiation of these cells without affecting cell viability [5].
• While TPA and dibutyryl-cyclic AMP have no detectable effect, ammonium vanadate induces tyrosine and threonine phosphorylation in S-MAG [6].
• Female B6C3F1 mice were given intraperitoneal injections of ammonium metavanadate (2.5 or 10 mg V/Kg), ammonium chloride, or sodium phosphate buffer every 3 days for 6 weeks [7].
• Double endoreduplication of Chinese hamster CHO-K1 cells that exhibited quadruple chromosomes at metaphase was induced by a combination of rotenone and ammonium vanadate treatments [8].
• Vanadium oxide nanotubes were synthesized as the main product by hydrothermal self-assembling from ammonium metavanadate (NH(4)VO(3)) and organic molecules as structure-directing templates [9].

Chemical compound and disease context of Ammonium monovanadate

• It is thus concluded that ammonium metavanadate, vanadyl sulphate, and bis(maltolato) oxovanadium (i.v.), at least at the doses and at the duration of treatment employed, do not produce significant haematological toxicity in rats [10].

Biological context of Ammonium monovanadate

• Ammonium metavanadate was studied for its ability to induce mitotic gene conversion and reverse point mutation in the D7 strain of Saccharomyces cerevisiae [11].
• Oxidative stress-regulated gene expression and promotion of morphological transformation induced in C3H/10T1/2 cells by ammonium metavanadate [12].
• The pentavalent vanadium compound ammonium metavanadate was shown previously to disrupt cell-mediated immunity at the earliest stages of an in vivo anti-Listerial response, in that mice treated with vanadium displayed decreased accessory cell recruitment and numbers of activated macrophages at infection sites [13].
• Modulation of macrophage activation by ammonium metavanadate [14].
• The present study was an attempt to assess the effect of vanadium (ammonium monovanadate) on cell proliferation, apoptosis and histopathology in the mammary tissue [15].

Anatomical context of Ammonium monovanadate

• Modulation of Fc tau receptor expression and function in mouse peritoneal macrophages by ammonium metavanadate [16].
• Expression pattern of heat shock proteins (Hsp) 72/73 and glucose regulated protein (Grp) 94 was studied in liver, kidney and testis of rats injected with sublethal doses of ammonium metavanadate (5 mg/kg/day) [17].
• Ammonium vanadate (NH4VO3; 50-1000 microM) increases the force of contraction of isolated electrically driven cat papillary muscles in a concentration-dependent manner [18].
• An inhibitor of tyrosine phosphatase, ammonium vanadate, increased the amount of radioactive phosphate in MAG several fold in both oligodendrocytes and Schwann cells [19].
• The present study examined the effect, in vitro, of therapeutic concentrations of carbamazepine on the inhibition by ammonium metavanadate of the Na-K ATPase of erythrocytes from normal and from manic depressive subjects [20].

Associations of Ammonium monovanadate with other chemical compounds

• Proliferin transcripts were induced 40- to 100-fold by 20 microM ammonium metavanadate, 20-fold by 5 microM vanadium pentoxide but only three-fold by vanadium oxide sulfate [12].
• Paraffin sections of the brain fixed in ethanol-formalin-acetic acid mixture are stained in 0.1% acid fuchsin containing 0.125% of ammonium metavanadate and 1% of glacial acetic acid, differentiated if overstained in 0.01% of borax solution, and counterstained with 0.05-0.025% of toluidine blue in acetate buffer (pH 3.3) or Gill's II hematoxylin [21].

Gene context of Ammonium monovanadate

• Differential inhibition of IL-1 alpha and TNF-alpha generation by ammonium metavanadate in murine macrophages [22].
• Ammonium metavanadate yielded a dose-dependent increase in mutation frequency at the V79 hprt locus following a 24-h exposure period in serum-free F12 medium [23].
• Consistent with its response to other oxidant chemicals, induction of proliferin by ammonium metavanadate was inhibited almost completely by the antioxidant N-acetylcysteine (8 mM) [12].
• In vivo inhibition of the cerebral glutathione reductase was caused by ammonium metavanadate (12.5 mg/kg; three times a week for 6 weeks) [24].
• The phosphorylation can be augmented with the protein tyrosine phosphatase inhibitor ammonium vanadate and with TPA (an activator of protein kinase C) [25].

Analytical, diagnostic and therapeutic context of Ammonium monovanadate

• Haematological effects of oral administration of ammonium metavanadate 0.19 mmol V/kg/day, vanadyl sulphate 0.15 mmol V/kg/day, and bis(maltolato)oxovanadium (i.v.) 0.18 mmol V/kg/day in drinking water for 12 weeks were investigated in Wistar rats [10].

References