Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration. | - CCMAR -

Journal Article

TitleVanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration.
Publication TypeJournal Article
AuthorsSoares, SS, Martins, H, Duarte, RO, Moura, JJG, Coucelo, J, Gutiérrez-Merino, C, Aureliano, M
Year of Publication2007
JournalJ Inorg Biochem
Volume101
Issue1
Date Published2007 Jan
Pagination80-8
ISSN0162-0134
KeywordsAnimals, Biomarkers, Catalase, Lipid Peroxidation, Magnetic Resonance Spectroscopy, Oxidative Stress, Sea Bream, Subcellular Fractions, Superoxide Dismutase, Vanadates
Abstract

The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1mM 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 12h 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 12h after metavanadate administration, whilst for decavanadate no effects were observed except 1h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (-55%) mitochondrial CAT activity. At early times of exposure, 1 and 6h, 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.

DOI10.1016/j.jinorgbio.2006.08.002
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/17030392?dopt=Abstract

Alternate JournalJ. Inorg. Biochem.
PubMed ID17030392