Karachitos Andonis, Galganska Hanna, Wojtkowska Malgorzata, Budzinska Malgorzata, Stobienia Olgierd, Bartosz Grzegorz, Kmita Hanna
Laboratory of Bioenergetics, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Umultowska 89, 61-614 Poznan, Poland.
FEBS Lett. 2009 Jan 22;583(2):449-55. doi: 10.1016/j.febslet.2008.12.045. Epub 2008 Dec 29.
Available data suggest that a copper-and zinc-containing dismutase (CuZnSOD) plays a significant role in protecting eukaryotic cells against oxidative modifications which may contribute to cell aging. Here we demonstrated that depletion of CuZnSOD in Saccharomyces cerevisiae cells (Deltasod1 cells) affected distinctly channel activity of VDAC (voltage dependent anion selective channel) and resulted in a moderate reduction in VDAC levels as well as in levels of protein crucial for VDAC import into mitochondria, namely Tob55/Sam50 and Tom40. The observed alterations may result in mitochondriopathy and subsequently in the shortening of the replicative life span observed for S. cerevisiaeDeltasod1 cells.
现有数据表明，一种含铜和锌的超氧化物歧化酶（CuZnSOD）在保护真核细胞免受可能导致细胞衰老的氧化修饰方面发挥着重要作用。在此我们证明，酿酒酵母细胞中CuZnSOD的缺失（Deltasod1细胞）显著影响了电压依赖性阴离子选择性通道（VDAC）的通道活性，并导致VDAC水平以及对VDAC导入线粒体至关重要的蛋白质水平适度降低，即Tob55/Sam50和Tom40。观察到的这些改变可能导致线粒体病，进而导致酿酒酵母Deltasod1细胞的复制寿命缩短。
