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Vanadium stimulates mitochondrial ROS production in different ways

Zhe Shi, Hui-Xue Liu*, Xiao-Da Yang*   

  1. State Key Laboratory of Natural and Biomimetic Drugs; Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
  • Received:2011-05-11 Revised:2011-07-10 Online:2011-09-20 Published:2011-09-20
  • Contact: Hui-Xue Liu*, Xiao-Da Yang*

Abstract:

Vanadium compounds show potential in diabetes and cancer treatment, although the toxicity remains a great concern. Previous studies have shown that vanadium-induced oxidative stress affecting mitochondrial function is intensively responsible for the toxicity. In this work, we investigated the effects of the vanadium compounds sodium metavanadate (NaVO3) and vanadyl acetylacetonate (VO(acac)2) on mitochondrial ROS generation and respiratory complex activities. The experimental results showed that vanadium compounds affected the ROS generation and complex activities in different patterns depending on the chemical species. NaVO3 inhibited mitochondrial complexes I and II activities and stimulated ROS generation at low concentration range; while VO(acac)2 promoted complex II activity but resulted in electron leakage from the complex I-involved pathway. The present results provide new evidence for understanding the toxicity of antidiabetic vanadium compounds.

Key words: Vanadium species, ROS generation, Respiratory complex activity, Mitochondria

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