sod1 is essential for the viability of dt40 cells and nuclear sod1 functions as a guardian of genomic dnasod1 dt40细胞的生存能力是至关重要的,核sod1功能基因组dna的监护人.pdfVIP

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sod1 is essential for the viability of dt40 cells and nuclear sod1 functions as a guardian of genomic dnasod1 dt40细胞的生存能力是至关重要的,核sod1功能基因组dna的监护人.pdf

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sod1 is essential for the viability of dt40 cells and nuclear sod1 functions as a guardian of genomic dnasod1 dt40细胞的生存能力是至关重要的,核sod1功能基因组dna的监护人

SAGE-Hindawi Access to Research Journal of Nucleic Acids Volume 2010, Article ID 795946, 11 pages doi:10.4061/2010/795946 Research Article SOD1 Is Essential for the Viability of DT40 Cells and Nuclear SOD1 Functions as a Guardian of Genomic DNA Eri Inoue,1 Keizo Tano,2 Hanako Yoshii,2 Jun Nakamura,3 Shusuke Tada,1 Masami Watanabe,2 Masayuki Seki,1 and Takemi Enomoto1, 4 1 Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan 2 Research Reactor Institute, Kyoto University, Kumatori 590-0494, Japan 3 Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA 4 Research Institute of Pharmaceutical Sciences, Faculty of Pharmacy, Musashino University, 1-1-20 Shinmachi, Nishitokyo-shi, Tokyo 202-8585, Japan Correspondence should be addressed to Masayuki Seki, seki@mail.pharm.tohoku.ac.jp and Takemi Enomoto, t eno@musashino-u.ac.jp Received 19 April 2010; Accepted 4 June 2010 Academic Editor: Shigenori Iwai Copyright © 2010 Eri Inoue et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Reactive oxygen species (ROSs) are produced during normal cellular metabolism, particularly by respiration in mitochondria, and these ROSs are considered to cause oxidative damage to macromolecules, including DNA. In our previous paper, we found no indication that depletion of mitochondrial superoxide dismutase, SOD2, resulted in an increase in DNA damage. In this paper, we examined SOD1, which is distributed in