Abstract
Manganese superoxide dismutase (MnSOD) scavenges toxic superoxide radicals produced in the mitochondria. Transfection of the human MnSOD gene into mouse C3H 10T1/2 cells resulted in production of active MnSOD, which was properly transported into mitochondria. Overexpression of MnSOD protected cells from radiation-, but not chemically-induced neoplastic transformation. This finding demonstrates that oxidative stress that occurs in the mitochondria plays an important role in the development of neoplastic transformation.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Line
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Cell Transformation, Neoplastic / metabolism*
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Dose-Response Relationship, Radiation
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Free Radical Scavengers
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Gamma Rays
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Humans
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Mice
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Mice, Inbred C3H
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Microscopy, Immunoelectron
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Mitochondria / enzymology*
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Mitochondria / ultrastructure
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Neoplasm Transplantation
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Neoplasms, Radiation-Induced / pathology
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Neoplasms, Radiation-Induced / prevention & control*
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Sarcoma, Experimental / pathology
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Sarcoma, Experimental / prevention & control*
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Superoxide Dismutase / genetics
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Superoxide Dismutase / metabolism*
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Transfection
Substances
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Free Radical Scavengers
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Superoxide Dismutase