Author(s):
Soares, S. S. 
; Gutiérrez-Merino, Carlos ; Aureliano, M.
Date: 2007
Persistent ID: http://hdl.handle.net/10400.1/1301
Origin: Sapientia - Universidade do Algarve
Subject(s): Oxidative stress; Vanadium
Document details
Decavanadate toxicity effects following in vivo administration
Description
Very few in vivo animal studies involving vanadium consider the contribution of decavanadate (V10) to vanadium biological effects. Recently, it is been suggested that decameric vanadate may not completely fall apart into other vanadate oligomers before induces changes in cell homeostasis, namely in several stress markers. An acute exposure of different fish species (Halobactrachus didactilus, Lusitanian toadfish, and Sparus aurata, gilthead seabream) to decavanadate, but not to other vanadate oligomers, induced different effects than vanadate 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 Sparus aurata mitochondria in particular when decavanadate is administrated. Moreover, exposure to different vanadate oligomers induced morphological changes in fish cardiac, hepatic and renal tissues causing tissues lesions in the liver and kidney, but not cardiac tissue. Nevertheless, the results highlight that different vanadate oligomers seem to follow, not only in vitro but also in vivo, different pathways, with different targets and effects. These recent findings, that are now summarized, point out the decameric vanadate species contributions to in vivo effects induced by vanadium in biological systems.
Very few in vivo animal studies involving vanadium consider the contribution of decavanadate (V10) to vanadium biological effects. Recently, it is been suggested that decameric vanadate may not completely fall apart into other vanadate oligomers before induces changes in cell homeostasis, namely in several stress markers. An acute exposure of different fish species (Halobactrachus didactilus, Lusitanian toadfish, and Sparus aurata, gilthead seabream) to decavanadate, but not to other vanadate oligomers, induced different effects than vanadate 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 Sparus aurata mitochondria in particular when decavanadate is administrated. Moreover, exposure to different vanadate oligomers induced morphological changes in fish cardiac, hepatic and renal tissues causing tissues lesions in the liver and kidney, but not cardiac tissue. Nevertheless, the results highlight that different vanadate oligomers seem to follow, not only in vitro but also in vivo, different pathways, with different targets and effects. These recent findings, that are now summarized, point out the decameric vanadate species contributions to in vivo effects induced by vanadium in biological systems.
Document Type
Part of book or chapter of book
Language English
Language English
| Financiadores do RCAAP | |||||||
|
|
|
|
|
|
||