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S S Soares

Publications and source records attributed to S S Soares.

6 recordsLinked to original sources

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

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.

Animals↗

Vanadium distribution following decavanadate administration.

An acute exposure of two vanadate solutions-metavanadate and decavanadate-containing different vanadate oligomers, induces different patterns of subcellular vanadium distribution in blood plasma, red blood cells (RBC), and cardiac muscle subcellular fractions of the fish Sparus aurata (gilthead seabream). The highest amount of vanadium was found in blood plasma 1 h after (5 mM) intravenous vanadate administration (295 +/- 64 and 383 +/- 104 microg V/g dry tissue, for metavanadate and decavanadate solutions, respectively), being 80-fold higher than in RBC. After 12 h of administration, the amount of vanadium in plasma, as well as in cardiac cytosol, decreased about 50%, for both vanadate solutions. During the period between 1 and 12 h, the ratio of vanadium in plasma/vanadium in RBC increased from 27 to 128 for metavanadate, whereas it remains constant (77) for decavanadate. Both vanadium solutions were primarily accumulated in the mitochondrial fraction (138 +/- 0 and 195 +/- 34 ng V/g dry tissue for metavanadate and decavanadate solutions, respectively, after 12 h exposure), rather than in cytosol. The amount of vanadium in cardiac mitochondria was twofold higher than in cytosol, earlier for metavanadate (6 h) than for decavanadate (12 h). It is concluded that, in fish cardiac muscle, the vanadium distribution is dependent on the administration of decameric vanadate, with vanadium being mainly distributed in plasma, before being accumulated into the mitochondrial fraction.

Animals↗

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

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 microg V(-1) 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.

Animals↗

Cadmium and vanadate oligomers effects on methaemoglobin reductase activity from Lusitanian toadfish: in vivo and in vitro studies.

Cadmium and two vanadate solutions as 'metavanadate' (containing ortho and metavanadate species) and 'decavanadate' (containing decameric species) (5 mM) were injected intraperitoneously in Halobatrachus didactylus (Lusitanian toadfish), in order to evaluate the effects of cadmium and oligomeric vanadate species on methaemoglobin reductase activity from fish red blood cells. Following short-term exposure (1 and 7 days), different changes were observed on enzyme activity. After 7 days of exposure, 'metavanadate' increased methaemoglobin reductase activity by 67% (P < 0.05), whereas, minor effects were observed on enzymatic activity upon cadmium and 'decavanadate' administration. However, in vitro studies indicate that decameric vanadate, in concentrations as low as 50 microM, besides strongly inhibiting methaemoglobin reductase activity, promotes haemoglobin oxidation to methaemoglobin. Although decameric vanadate species showed to be unstable in the different media used in this work, the rate of decameric vanadate deoligomerization is in general slow enough, making it possible to study its effects. It is concluded that the increase in H. didactylus methaemoglobin reductase activity is more pronounced upon exposition to 'metavanadate' than to cadmium and decameric species. Moreover, only decameric vanadate species promoted haemoglobin oxidation, suggesting that vanadate speciation is important to evaluate in vivo and in vitro effects on methaemoglobin reductase activity.

Animals↗

Kaempferol glycosides from Siparuna apiosyce.

The kaempferol derivative 3,7-di-O-methyl-4'-O-beta-[alpha rhamnosyl (1 --> 6)]-glucopyranoside (siparunoside) was isolated from the leaves of Sparuna apiosyce. Its structure was established by extensive NMR studies. The alkaloids reticuline and liriodenine were also isolated from the leaves along with the kaempferol derivative tiliroside. Benzylisoquinoline alkaloids were isolated from the wood (liriodenine) and wood bark (liriodenine, laurotetanine, N-methyl-laurotetanine, reticuline), together with a mixture of cis and trans-N-feruloyltyramines. 3,7,4'-tri-O-methylkaempferol was isolated from all organs.

Chromatography, High Pressure Liquid↗

Chemistry and pharmacology of Monimiaceae: a special focus on Siparuna and Mollinedia.

The chemistry and pharmacology of species of the family Monimiaceae are reviewed, with special attention given to the genera Mollinedia and Siparuna, the two most important and representative in Brazil. The isolation of benzylisoquinoline alkaloids and kaempferol derivatives from Siparuna apiosyce is reported, as well as the isolation of aporphines from the fruits of Siparuna arianeae. Cinnamic acid derivatives and a gamma-lactone were isolated from Mollinedia gilgiana and Mollinedia marliae.

Alkaloids↗