Mechanisms of vanadate-induced cellular toxicity: role of cellular glutathione and NADPH

Capella, Luiz Sabbatini; Gefé, M.; Silva, Edson F.; Affonso-Mitidieri, O. R.; Lopes, Anibal Gil; Rumjanek, Vivian M.; Capella, Marcia A. M.

doi:10.1016/s0003-9861(02)00408-3

Cited by 72 publications

(65 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1). Even though vanadium may participate in Fenton-like reactions [9], together with the proposed mechanisms of vanadate action that involves its bioreduction and ROS production [15,18,19,40], our results point out to a depression in the overall rate of ROS production. This observation is in good agreement with previous reports showing that vanadate supplementation diminished oxidative stress in certain experimental conditions, such as in rat-induced hepatocarcinogenesis [23] and in rat diabetic tissues [41].…”

Section: Resultsmentioning

confidence: 61%

“…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%

“…Thus, decameric vanadate species induced changes in O ÅÀ 2 mitochondrial production opposite to those produced by the oligomeric vanadate species that are present in metavanadate solution, from which we can suggest again different pathways of biological action for the different oligomers. Several proposed vanadate action pathways within cells involves O ÅÀ 2 production mediated by NADPH oxido-reductases from the respiratory chain [15,18,19,40]. If we consider the action and detoxification mechanism proposed for vanadate, where vanadate is reduced to vanadyl with production of O ÅÀ 2 , it is possible that decavanadate participates in such reactions in a different manner.…”

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 3 more Smart Citations

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: 61%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

“…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

106

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

Essential and Toxic Effects of Elements on Microorganisms

Nies¹

2004

Elements and Their Compounds in the Environment

View full text Add to dashboard Cite

Mechanisms of vanadate-induced cellular toxicity: role of cellular glutathione and NADPH

Cited by 72 publications

References 35 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

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

Essential and Toxic Effects of Elements on Microorganisms

Contact Info

Product

Resources

About