Takada Shunya, Inoue Eri, Tano Keizo, Yoshii Hanako, Abe Takuya, Yoshimura Akari, Akita Motomu, Tada Shusuke, Watanabe Masami, Seki Masayuki, Enomoto Takemi
Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan.
Biochem Biophys Res Commun. 2009 Feb 6;379(2):233-8. doi: 10.1016/j.bbrc.2008.12.031. Epub 2008 Dec 25.
Manganese-dependent superoxide dismutase (SOD2) serves as the primary defense against mitochondrial superoxide, and decreased SOD2 activity results in a range of pathologies. To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox). When SOD2 was depleted by the addition of Dox, the cells grew slightly slower and formed fewer colonies than cells expressing hSOD2. In addition, these cells showed a high sensitivity to paraquat, which produces superoxide, and died through apoptosis. In contrast to results obtained with mouse and DrosophilaSod2 mutants, we found no indication of an increase in DNA lesions due to depletion of SOD2.
锰依赖性超氧化物歧化酶（SOD2）是抵御线粒体超氧化物的主要防线，SOD2活性降低会导致一系列病理状况。为了研究SOD2缺失后不久发生的事件，我们构建了用人类SOD2（hSOD2）cDNA互补的SOD2基因敲除鸡DT40细胞，其表达可通过强力霉素（Dox）关闭。当通过添加Dox使SOD2缺失时，与表达hSOD2的细胞相比，这些细胞生长略慢且形成的集落更少。此外，这些细胞对产生超氧化物的百草枯表现出高度敏感性，并通过凋亡死亡。与在小鼠和果蝇Sod2突变体中获得的结果相反，我们没有发现因SOD2缺失导致DNA损伤增加的迹象。
