© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 23, 1818-1821,
December 5, 2001
© 2001 Oxford University Press
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Manganese Superoxide Dismutase Alanine-to-Valine Polymorphism at Codon 16 and Lung Cancer Risk
Affiliations of authors: L. I. Wang (Department of Epidemiology) D. P. Miller, Y. Sai, L. Su (Department of Environmental Health, Occupational Health Program), Harvard School of Public Health, Boston, MA; G. Liu, Department of Environmental Health, Occupational Health Program, Harvard School of Public Health, and Hematology–Oncology Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston; J. C. Wain, Thoracic Surgery Unit, Department of Surgery, Department of Medicine, Massachusetts General Hospital, Harvard Medical School; T. J. Lynch, Hematology–Oncology Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School; D. C. Christiani, Department of Epidemiology and Department of Environmental Health, Occupational Health Program, Harvard School of Public Health, and Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School.
Correspondence to: David C. Christiani, M.D., M.P.H., Occupational Health Program, Harvard School of Public Health, 665 Huntington Ave., Bldg. 1, Rm. 1402, Boston, MA 02115 (e-mail: dchris@hohp.harvard.edu).
Manganese superoxide dismutase (MnSOD) catalyzes the dismutation of a specific type of reactive oxygen species, superoxide radicals, into hydrogen peroxide and oxygen (1). Accumulation of reactive oxygen species can damage DNA, proteins, and lipids, leading to the initiation or promotion of cancer (2,3). MnSOD, the only known superoxide scavenger in mitochondria, may be particularly important for antioxidant defense because mitochondria are the major sites for cellular metabolism and hence production of reactive oxygen species (4).
The signal sequence is essential for correct transport and processing of proteins by mitochondria (5). Indirect evidence suggests that the alanine-to-valine polymorphism at codon 16 (Ala16Val) in the signal sequence of MnSOD (5), also described as the –9 position (6), produces a conformational change in the helical structure of the protein. This change may decrease the efficiency
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