Aureliano M, Ohlin C André
DCBB, Faculty of Sciences and Technology, University of Algarve, Campus de Gambelas, 8005-135 Faro, Portugal; CCMar, University of Algarve, Campus de Gambelas, 8005-135 Faro, Portugal.
School of Chemistry, Monash University, Clayton, Victoria 3800, Australia.
J Inorg Biochem. 2014 Aug;137:123-30. doi: 10.1016/j.jinorgbio.2014.05.002. Epub 2014 May 14.
This review covers recent advances in the understanding of the in vitro and in vivo effects of decavanadate, (V10O28)(6-), particularly in mitochondria. In vivo toxicological studies involving vanadium rarely account for the fact that under physiological conditions some vanadium may be present in the form of the decavanadate ion, which may behave differently from ortho- and metavanadates. It has for example been demonstrated that vanadium levels in heart or liver mitochondria are increased upon decavanadate exposure. Additionally, in vitro studies have shown that mitochondrial depolarization (IC50, 40 nM) and oxygen consumption (IC50, 99 nM) are strongly affected by decavanadate, which causes reduction of cytochrome b (complex III). We review these recent findings which together suggest that the observed cellular targets, metabolic pathway and toxicological effects differ according to the species of vanadium present. Finally, the toxicological effects of decavanadate depend on several factors such as the mode of administration, exposure time and type of tissue.
本综述涵盖了对十钒酸盐（V10O28）(6-)的体外和体内效应，特别是在线粒体中的效应的最新研究进展。涉及钒的体内毒理学研究很少考虑到在生理条件下，一些钒可能以十钒酸根离子的形式存在，其行为可能与正钒酸盐和偏钒酸盐不同。例如，已经证明，暴露于十钒酸盐后，心脏或肝脏线粒体中的钒含量会增加。此外，体外研究表明，十钒酸盐会强烈影响线粒体去极化（IC50，40 nM）和氧消耗（IC50，99 nM），它会导致细胞色素b（复合体III）的还原。我们回顾了这些最新发现，这些发现共同表明，根据存在的钒的种类不同，观察到的细胞靶点、代谢途径和毒理学效应也不同。最后，十钒酸盐的毒理学效应取决于几个因素，如给药方式、暴露时间和组织类型。
