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Vanadate
About: Vanadate is a research topic. Over the lifetime, 4497 publications have been published within this topic receiving 120109 citations. The topic is also known as: vanadate.
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TL;DR: Data suggest that the oxidation state and coordination geometry of vanadium determine the degree of the cytotoxic-like effect of the vanadium compounds.
Abstract: Vanadium compounds are shown to have a mitogenic effect on fibroblast cells. The effects of vanadate, vanadyl and pervanadate on the proliferation and morphological changes of Swiss 3T3 cells in culture are compared. Vanadium derivatives induced cell proliferation in a biphasic manner, with a toxic-like effect at doses over 50mM, after 24h of incubation. Vanadyl and vanadate were equally potent at 2.5–10mM. At 50mM vanadate inhibited cell proliferation, whereas slight inhibition was observed at 100mM of vanadyl. At 10mM pervanadate was as potent as vanadate and vanadyl in stimulating fibroblast proliferation, but no effect was observed at lower concentrations. A pronounced cytotoxic-like effect was induced by pervanadate at 50mM. All of these effects were accompanied by morphological changes: transformation of fibroblast shape from polygonal to fusiform; retraction with cytoplasm condensation; and loss of lamellar processes. The magnitude of these transformations correlates with the potency of vanadium derivatives to induce a cytotoxic-like effect: pervanadate>vanadate>vanadyl. These data suggest that the oxidation state and coordination geometry of vanadium determine the degree of the cytotoxicity.
38 citations
TL;DR: The ability of living Trypanosoma rangeli Mg-dependent ecto-ATPase activity was insensitive to inhibitors of other ATPase and phosphatase activities, such as oligomycin, sodium azide, bafilomycin A1, ouabain, furosemide, vanadate, molybdate, sodium fluoride, tartrate, and levamizole.
38 citations
TL;DR: It is proposed that radical formation originates from reduction of O2 by NADPH, analogous to processes described in microsomal membranes, and vanadate and ferricyanide are probably required to amplify the peroxidative reaction sufficiently to overcome the cellular antioxidative capacity.
38 citations
TL;DR: In this paper, the vanadate film with better corrosion resistance forms on Mg-Li-Al-Ce surface after the sample is immersed in 30 g L −1 NH 4 VO 3 ǫ+3.75 g L−1 K 3 (Fe(CN) 6 ) solution at 80°C for 10 min.
38 citations
TL;DR: It is concluded that both insulin and vanadate follow the same signalling pathway downstream of PI 3-kinase to stimulate 2-deoxy-D-glucose transport.
Abstract: It is now widely accepted that insulin stimulation of glucose uptake by muscle cells is due to the activation of protein kinase B, leading to the recruitment of glucose transporter proteins from an intracellular compartment to the plasma membrane. Vanadate is a protein tyrosine phosphatase (PTP) inhibitor and a known insulin mimetic agent. Vanadate causes an increase of glucose transport in various tissues, but the mechanism of stimulation is not clearly understood. Hence in the present study, we have compared the mechanism of 2-deoxy-D-glucose transport induced by vanadate and insulin in isolated rat cardiomyocytes. Vanadate stimulated deoxyglucose transport in a time- and concentration-dependent manner. Insulin (100 nM) and vanadate (5 mM) stimulated 2-deoxy-D-glucose transport on an average by 3- and 2-fold respectively over basal values. The stimulation of glucose transport was accompanied by an activation of protein kinase B (PKB). This study also revealed that the activation of PKB and stimulation of 2-deoxyglucose uptake by vanadate and insulin are inhibited by treatment with wortmannin, a specific inhibitor of phoshatidylinositol 3-kinase (PI 3-kinase). Hence, we conclude that both insulin and vanadate follow the same signalling pathway downstream of PI 3-kinase to stimulate 2-deoxy-D-glucose transport.
38 citations