Soares S S, Martins H, Duarte R O, Moura J J G, Coucelo J, Gutiérrez-Merino C, Aureliano M
CCMAR, Universidade do Algarve, Campus de Gambelas, 8005-139 Faro, Portugal.
J Inorg Biochem. 2007 Jan;101(1):80-8. doi: 10.1016/j.jinorgbio.2006.08.002. Epub 2006 Aug 30.
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.
在金头鲷静脉注射十钒酸盐溶液（总钒浓度为1 mM）后，研究了十聚钒酸盐物种对心肌钒中毒效应的影响。尽管十聚钒酸盐在测定介质中不稳定，其分解半衰期为16，这使得不仅可以在体外而且可以在体内研究其作用。与注射含不稳定氧钒酸盐的偏钒酸盐溶液相比，注射十钒酸盐后1、6和12小时，血浆、红细胞以及心脏线粒体和细胞溶质中钒的增加不受影响。偏钒酸盐注射后1、6和12小时，心脏组织脂质过氧化增加高达20%，而对于十钒酸盐，除治疗后1小时（增加20%）外未观察到影响。偏钒酸盐注射与十钒酸盐明显不同，暴露12小时后，前者增强线粒体超氧化物歧化酶（SOD）活性（增加115%）且不影响过氧化氢酶（CAT）活性，而十钒酸盐使SOD活性增加20%并降低（降低55%）线粒体CAT活性。在暴露早期，即1和6小时，注射十钒酸盐后观察到的唯一影响是SOD活性增加20%。总之，尽管注射十钒酸盐和偏钒酸盐后在心脏细胞中观察到相同的钒分布，但十钒酸盐在脂质过氧化和氧化应激标志物方面具有不同的反应模式。有人认为，一旦形成，十聚钒酸盐物种具有与钒酸盐不同的反应性，因此，指出在解释钒酸盐的体内毒性时应考虑钒低聚物的不同贡献。
