Vanadium in cancer treatment

Evangelou, Angelos

doi:10.1016/s1040-8428(01)00221-9

Cited by 569 publications

(430 citation statements)

References 146 publications

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“…There are many divergent data resulting from the fact that biological activity of vanadium depends on factors such as: the type of the derivative, manner of its administration, dose, length of treatment, and also individual and species specific sensitivity to the administered compound. The toxicity of vanadium is correlated to its degree of oxidation (vanadyl < vanadate ion) and chemical form (organic < inorganic ligand) [16,42]. This was demonstrated by experiments on animals, mainly in rats and mice [9,42,[60][61][62].…”

Section: Toxicity Of Vanadiummentioning

confidence: 97%

“…Their ratio depends mainly on the pH value of the intracellular environment: in the neutral pH, for example, there is a rapid polymerization of monomers to hexamers, while dekamers emerge in acidic pH [16]. The polymers of vanadate ions form complexes with proteins, and can therefore influence the cell metabolism [17,18].…”

Section: The Overall Metabolism Of Vanadiummentioning

confidence: 99%

“…Fig. 1 Potential vanadium-induced cellular oxidative stress (see [16,21]); SOD -superoxide dysmutase.…”

Section: The Overall Metabolism Of Vanadiummentioning

confidence: 99%

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Biological activity of vanadium compounds

Goc

2006

Open Life Sciences

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Vanadium compounds are characterised by a broad spectrum of action in vivo and in vitro. Their insulin-mimetic activity is manifested in their ability to normalize changes observed in both clinical and experimental diabetes (i.e. hyperglycaemia, hyperlipidaemia, lowered cell sensitivity to insulin) through the regulation of carbohydrate and lipid metabolism and the removal of secondary symptoms of this disease (as e.g. retinopathy, cardiomyopathy, nephropathy). Nevertheless, vanadium is considered to be a toxic element in both cationic and anionic form, although the latter type has more serious side effects. This is accounted for by the faster absorption of anionic forms, although the chemical structure, geometry, and the manner of synthesis of its derivatives also contributes to this elevated toxicity. Besides their antidiabetic properties, vanadium derivatives have also been observed to influence processes related to mitogenic cell responses (apoptosis, proliferation, neoplastic transformation). However, both anti-and pro-neoplastic properties of vanadium are reported.

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Section: Toxicity Of Vanadiummentioning

confidence: 97%

Section: The Overall Metabolism Of Vanadiummentioning

confidence: 99%

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Biological activity of vanadium compounds

Goc

2006

Open Life Sciences

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“…Moreover, vanadium toxicological effects in several cell types have been related with ROS production [16][17][18][19]. Nevertheless, vanadium was recently reviewed as ''an element of atypical biological significance'' [20], due to insulin mimetic properties of vanadium [16,21,22] and to the preventive effects of vanadium against animal carcinogens [23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Gândara

Soares

Martins

et al. 2005

Journal of Inorganic Biochemistry

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The formation of vanadate oligomeric species is often disregarded in studies on vanadate effects in biological systems, particularly in vivo, even though they may interact with high affinity with many proteins. We report the effects in fish hepatic tissue of an acute intravenous exposure (12, 24 h and 7 days) to two vanadium(V) solutions, metavanadate and decavanadate, containing different vanadate oligomers administered at sub-lethal concentration (5 mM; 1 mg/kg). Decavanadate solution promotes a 5-fold increase (0.135 ± 0.053 lg V À1 dry tissues) in the vanadium content of the mitochondrial fraction 7 days after exposition, whereas no effects were observed after metavanadate solution administration. Reduced glutathione (GSH) levels did not change and the overall reactive oxygen species (ROS) production was decreased by 30% 24 h after decavanadate administration, while for metavanadate, GSH levels increased 35%, the overall ROS production was depressed by 40% and mitochondrial superoxide anion production decreased 45%. Decavanadate intoxication did not induce changes in the rate of lipid peroxidation till 12 h, but later increased 80%, which is similar to the increase observed for metavanadate after 24 h. Decameric vanadate administration clearly induces different effects than the other vanadate oligomeric species, pointing out the importance of taking into account the different vanadate oligomers in the evaluation of vanadium(V) effects in biological systems.

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“…The mechanisms underlying the antitumour properties of this metal and its compounds remain unclear. Some of the following actions are probably related to its anticancer properties: 1) protective effect against the induction of DNA strand breaks and chromosome aberrations by potent hepatocarcinogens; 2) inhibition of metabolic activation of the procarcinogen, leading to reduced generation and/or binding of the ultimate carcinogen to DNA; 3) elevated detoxification of the precarcinogen and/or its reactive metabolites through specific induction of activities of some of the xenobiotic biotransforming enzymes; 4) inhibition of DNA polymerasaes, nucleotidyl transferases and phosphotransferas; 5) effect on the immune system [18][19][20][21][22]. Additional experiments are required to clarify better the possible involvement of vanadium in src signalling pathways.…”

mentioning

confidence: 99%

Ammonium Vanadate Decreases Viability and Proliferation Activity of Cultured Virustransformed Rat Sarcoma Cells

Abudalleh¹,

Alexandrov²,

Alexandrova³

2013

Proceeding BAS

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The aim of the study presented was to evaluate the effect of ammonium vanadate (NH 4 VO 3 ) on the viability and proliferation of cultured virustrasformed rat sarcoma LSR-SF-SR cells. The investigations were performed by MTT test, neutral red uptake cytotoxicity assay, double staining with acridine orange and propidium iodide, the method of Pappenheim and colony-forming technique. The results obtained revealed that applied at a concentration range of 0.1-20 µg/ml NH 4 VO 3 expresses significant cytotoxic and/or cytostatic effects that are time-and concentration-dependent.

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Vanadium in cancer treatment

Cited by 569 publications

References 146 publications

Biological activity of vanadium compounds

Biological activity of vanadium compounds

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Ammonium Vanadate Decreases Viability and Proliferation Activity of Cultured Virustransformed Rat Sarcoma Cells

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