Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10766326 | Biochemical and Biophysical Research Communications | 2009 | 6 Pages |
Abstract
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.
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Authors
Shunya Takada, Eri Inoue, Keizo Tano, Hanako Yoshii, Takuya Abe, Akari Yoshimura, Motomu Akita, Shusuke Tada, Masami Watanabe, Masayuki Seki, Takemi Enomoto,