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Overexpression of Mitochondrial Manganese Superoxide Dismutase Protects against Radiation-induced Cell Death in the Human Hepatocellular Carcinoma Cell Line HLE¹

Research Center of Charged Particle Therapy [S. M., H. K., F. H., H. T.], International Space Radiation Laboratory [H. J. M., S. K., C. Y.], Redox Research Group [T. O.], National Institute of Radiological Sciences, Chiba 263-8555, Japan; First Department of Medicine, Chiba University School of Medicine, Chiba, 260-0856, Japan [S. M., M. E., F. H., H. S.]; and Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan [T. N.]

We investigated the potential role of mitochondrial manganese superoxide dismutase (Mn-SOD) in protective activity against irradiation by analyzing cell viability by a colony formation assay and by detecting apoptosis in stably human Mn-SOD gene-transfected HLE, a hepatocellular carcinoma cell line. We found that overexpression of Mn-SOD reduced the levels of reactive oxygen species in the mitochondria and intracellular phospholipid peroxidation product (4-hydroxy-2-nonenal) and prevented cell death. The production of intracellular nitric oxide after irradiation was not changed by Mn-SOD overexpression. The results suggested that Mn-SOD might play an important role in protecting cells against radiation-induced cell death by controlling the generation of mitochondrial reactive oxygen species and intracellular lipid peroxidation.

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