Chemopreventive effects of vanadium toward 1,2‐dimethylhydrazine‐induced genotoxicity and preneoplastic lesions in rat colon

Kanna, P. Suresh; Mahendrakumar, C. B.; Indira, Bommi; Srivastawa, Sunil; Kalaiselvi, K.; Elayaraja, T.; Chatterjee, Mainak

doi:10.1002/em.20038

Cited by 31 publications

(16 citation statements)

References 24 publications

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“…Recent data indicate spermicidal and anti-HIV activity of vanadium compounds (D'Cruz et al 2003) and the use of these compounds for the treatment of diabetes (Heinemann et al 2003;Sakurai et al 2004;Yang et al 2004) as well as the prevention of animal carcinogens (Kanna et al 2004;Molinuevo et al 2004). It was reported that decavanadate (V 10 ) is the major protein-bound species of vanadium and have a stronger effect on various enzymes, when compared to other vanadate oligomers (Aureliano and Gândara 2005).…”

Section: Introductionmentioning

confidence: 99%

Influence of decavanadate on rat synaptic plasma membrane ATPases activity

Krstić¹,

Čolović²,

Bošnjaković-Pavlović³

et al. 2009

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Abstract.The in vitro influence of decameric vanadate species on Na + /K + -ATPase, plasma membrane Ca 2+ -ATPase (PMCA)-calcium pump and ecto-ATPase activity, using rat synaptic plasma membrane (SPM) as model system was investigated, whereas the commercial porcine cerebral cortex Na + /K + -ATPase served as a reference. The thermal behaviour of the synthesized decavanadate (V 10 ) has been studied by differential scanning calorimetry and thermogravimetric analysis, while the type of polyvanadate anion was identified using the IR spectroscopy. The concentration-dependent responses to V 10 of all enzymes were obtained. The half-maximum inhibitory concentration (IC 50 ) of the enzyme activity was achieved at (4.74 ± 1.15) × 10 -7 mol/l for SPM Na + /K + -ATPase, (1.30 ± 0.10) × 10 -6 mol/l for commercial Na + /K + -ATPase and (3.13 ± 1.70) × 10 -8 mol/l for Ca 2+ -ATPase, while ecto-ATPase is significantly less sensitive toward V 10 (IC 50 = (1.05 ± 0.10) × 10 -4 mol/l) than investigated P-type ATPases. Kinetic analysis showed that V 10 inhibited Na + /K + -ATPase by reducing the maximum enzymatic velocity and apparent affinity for ATP (increasing K m value), implying a mixed mode of interaction between V 10 and P-type ATPases.

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Section: Introductionmentioning

confidence: 99%

Influence of decavanadate on rat synaptic plasma membrane ATPases activity

Krstić¹,

Čolović²,

Bošnjaković-Pavlović³

et al. 2009

gpb

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“…It has been reported that vanadate reverses drug resistance [6,7], increases glucose metabolism [8] and influences the activity of several enzymes, either inhibiting or stimulating [9][10][11]. Recent data associated vanadium essentially to the treatment of diabetes, due to its insulin mimetic properties [12][13][14] and to the prevention of animal carcinogens [15,16], however some studies of DÕCruz and its collaborators have reported spermicidal and anti-HIV activity of vanadium compounds [17].…”

Section: Introductionmentioning

confidence: 99%

Decavanadate effects in biological systems

Aureliano

Gândara

2005

Journal of Inorganic Biochemistry

117

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Vanadium biological studies often disregarded the formation of decameric vanadate species known to interact, in vitro, with high-affinity with many proteins such as myosin and sarcoplasmic reticulum calcium pump and also to inhibit these biochemical systems involved in energy transduction. Moreover, very few in vivo animal studies involving vanadium consider the contribution of decavanadate to vanadium biological effects. Recently, it has been shown that an acute exposure to decavanadate but not to other vanadate oligomers induced oxidative stress and a different fate in vanadium intracellular accumulation. Several markers of oxidative stress analyzed on hepatic and cardiac tissue were monitored after in vivo effect of an acute exposure (12, 24 h and 7 days), to a sub-lethal concentration (5 mM; 1 mg/kg) of two vanadium solutions (''metavanadate'' and ''decavanadate''). It was observed that ''decavanadate'' promote different effects than other vanadate oligomers in catalase activity, glutathione content, lipid peroxidation, mitochondrial superoxide anion production and vanadium accumulation, whereas both solutions seem to equally depress reactive oxygen species (ROS) production as well as total intracellular reducing power. Vanadium is accumulated in mitochondria in particular when ''decavanadate'' is administered. These recent findings, that are now summarized, point out the decameric vanadate species contributions to in vivo and in vitro effects induced by vanadium in biological systems.

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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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Chemopreventive effects of vanadium toward 1,2‐dimethylhydrazine‐induced genotoxicity and preneoplastic lesions in rat colon

Cited by 31 publications

References 24 publications

Influence of decavanadate on rat synaptic plasma membrane ATPases activity

Influence of decavanadate on rat synaptic plasma membrane ATPases activity

Decavanadate effects in biological systems

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

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