Characterization of oxygen free radicals generated during vanadate-stimulated NADH oxidation

Kalyani, P.; Satchidanandam, Vijaya; Ramasarma, T.

doi:10.1007/bf00229571

Cited by 24 publications

(11 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). Since GSH was found to be involved in vanadate bioreduction [10][11][12][13][14][15], the levels of GSH should be affected when vanadate is administered. Indeed, it has been reported that the GSH pool is enhanced in the presence of vanadate [23,39].…”

Section: Resultsmentioning

confidence: 99%

“…Vanadium can induce the formation of reactive oxygen species (ROS) in biological systems through: (i) Fenton-like reactions [9]; (ii) vanadate bioreduction mediated by reduced glutathione (GSH), flavoenzymes or NAD(P)H oxidases with ROS as a by-product [10][11][12][13][14][15]; (iii) and recent evidences point out to an indirect promotion of ROS production, probably by interacting with mitochondria [16]. Moreover, vanadium toxicological effects in several cell types have been related with ROS production [16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Gândara

Soares

Martins

et al. 2005

Journal of Inorganic Biochemistry

View full text Add to dashboard Cite

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.

show abstract

Section: Resultsmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…Thus, vanadate has been reported to inhibit the generation of superoxide, resulting in a blunting of the superoxide-induced loss of sarcolemmal Ca 2ϩ pump activity and Na ϩ -dependent Ca 2ϩ uptake in isolated rat hearts (Matsubara et al, 1995). In contrast, under certain conditions in vitro, vanadate has been shown to be capable of generating free radicals (Kalyani et al, 1992). However, this does not account for all its actions because other investigators failed to observe any action of reductants or antioxidants on vanadate-induced expression of actin and c-Ha-ras (Yin et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

Liem

Gho²,

Gho³

et al. 2004

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

Vanadate has been shown to inhibit tyrosine phosphatase, leading to an increased tyrosine phosphorylation state. The latter has been demonstrated to be involved in the signal transduction pathway of ischemic preconditioning, the most potent endogenous mechanism to limit myocardial infarct size. Furthermore, there is evidence that phosphatase inhibition may be cardioprotective when given late after the onset of ischemia, but the mechanism of protection is unknown. We tested the hypothesis that the organic vanadate compound bis(maltolato)-oxovanadium (BMOV) limits myocardial infarct size by attenuating reperfusion injury and investigated the underlying mechanism. Myocardial infarction was produced in 112 anesthetized rats by a 60-min coronary artery occlusion, and infarct size was determined histochemically after 180 min of reperfusion. Intravenous infusion of BMOV in doses of 3.3, 7.5, and 15 mg/kg i.v. decreased infarct size dose-dependently from 70 Ϯ 2% of the area at risk in vehicle-treated rats down to 41 Ϯ 5% (P Ͻ 0.05 versus control), when administered before occlusion. Administration of the low dose just before reperfusion was ineffective, but administration of the higher doses was equally cardioprotective as compared with administration before occlusion. The cardioprotection by BMOV was abolished by the tyrosine kinase inhibitor genistein and by the ATP-sensitive potassium (K ϩ ATP ) channel blocker glibenclamide but was not affected by the ganglion blocker hexamethonium. We conclude that BMOV afforded significant cardioprotection principally by limiting reperfusion injury. The mode of action appears to be by opening of cardiac K ϩ ATP channels via increased tyrosine phosphorylation.

show abstract

“…Several biological studies associate vanadium with the ability to produce reactive oxygen species (ROS) resulting in antioxidant enzymes alterations and leading to lipid peroxidation [1][2][3][4][5][6][7][8]. The involvement of toxic metals in cardiac oxidative damage suggests that this organ shows a great vulnerability to metal intoxication [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Soares

Martins

Duarte

et al. 2007

Journal of Inorganic Biochemistry

110

View full text Add to dashboard Cite

The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1 mM total vanadium) in Sparus aurata. Although decameric vanadate is unstable in the assay medium, it decomposes with a half-life time of 16 allowing studying its effects not only in vitro but also in vivo. After 1, 6 and 12 h upon decavanadate administration the increase of vanadium in blood plasma, red blood cells and in cardiac mitochondria and cytosol is not affected in comparison to the administration of a metavanadate solution containing labile oxovanadates. Cardiac tissue lipid peroxidation increases up to 20%, 1, 6 and 12 h after metavanadate administration, whilst for decavanadate no effects were observed except 1 h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12 h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (À55%) mitochondrial CAT activity. At early times of exposure, 1 and 6 h, the only effect observed upon decavanadate administration was the increase by 20% of SOD activity. In conclusion, decavanadate has a different response pattern of lipid peroxidation and oxidative stress markers, in spite of the same vanadium distribution in cardiac cells observed after decavanadate and metavanadate administration. It is suggested that once formed decameric vanadate species has a different reactivity than vanadate, thus, pointing out that the differential contribution of vanadium oligomers should be taken into account to rationalize in vivo vanadate toxicity.

show abstract

Characterization of oxygen free radicals generated during vanadate-stimulated NADH oxidation

Cited by 24 publications

References 30 publications

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

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

The Tyrosine Phosphatase Inhibitor Bis(Maltolato)Oxovanadium Attenuates Myocardial Reperfusion Injury by Opening ATP-Sensitive Potassium Channels

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Contact Info

Product

Resources

About