作者: Simona Reina , Stefano Conti Nibali , Marianna F Tommasello , Cristiana Lipari , Iolanda Infantino
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摘要: Mitochondria are predominant source of intracellular reactive oxygen species (ROS) and exploit a wide range of antioxidant defense systems to fight against mitochondrial ROS-derived oxidative stress [1]. In addition to the well-known superoxide dismutases (SODs), GSH-PX and the PRX/Trx systems, we reported for the first time that the outer mitochondrial pore VDAC3 actively contributes to mitigate mitochondrial ROS levels [2]. VDAC is the main actor in controlling the metabolite and ion flux across the mitochondrial surface and participates to numerous cellular pathways including apoptosis [3]. Among the three VDAC isoforms that exists in mammals, VDAC3 has always been the least characterized. It is less expressed than VDAC1 and VDAC2 and exhibits tissue specificity for liver, brain, heart and spermatozoa. Moreover, it possesses peculiar biophysical features that have been attributed to the redox state of its …