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钒化合物在癌症及糖尿病治疗中显示出其潜在的可能而受到人们的关注,但是其毒性限制了其作为药物的进一步发展。已有研究表明钒通过影响线粒体功能诱导的氧化应激是钒化合物毒性的主要原因。本工作主要考察了两种钒化合物-偏钒酸钠和乙酰丙酮氧钒对线粒体活性氧产生和呼吸链复合体活性的影响。结果表明,钒化合物依其化学物种的不同而对活性氧和复合体活性以不同的方式产生影响。偏钒酸钠抑制线粒体复合体Ⅰ和Ⅱ的活性,同时在低浓度范围内促进活性氧的产生。而氧钒化合物则促进复合体Ⅱ活性,同时促进复合体Ⅰ相关途径的电子漏。本工作为研究钒化合物作为抗糖尿病药物毒性提供了新的结果。
Vanadium compounds have drawn much attention for their potential applications in the treatment of cancer and diabetes, but their toxicity limits their further development as drugs. It has been reported that oxidative stress induced by vanadium through mitochondrial function is the main reason for the toxicity of vanadium compounds. In this work, we investigated the effects of two vanadium compounds, sodium metavanadate and vanadyl acetylacetonate, on the production of mitochondrial ROS and the activity of respiratory chain complex. The results show that vanadium compounds affect the activity of reactive oxygen species and complex in different ways depending on their chemical species. Sodium metavanadate inhibits the activity of mitochondrial complexes I and II while promoting the production of reactive oxygen species at low concentrations. The vanadyl compounds promote the activity of complex II and promote the electron leakage of complex Ⅰ related pathways. This work provided new results for the study of vanadium compounds as anti-diabetic drugs.