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Recent studies have shown that homozygous Mn superoxide dismutase (Sod2) gene-knockout mice (Sod2-/-) die shortly after birth with extensive myocardial injury, whereas heterozygous mutants (Sod2+/-) are phenotypically normal in room air. In the current study, we showed that Sod2+/- mice with approximately 50% of normal pulmonary MnSOD activity and normal levels of lung CuZnSOD, catalase, and glutathione peroxidase activities were not substantially more susceptible to 100% O2 toxicity than their normal Sod2+/+ littermates. The mean (± SD) survival of Sod2+/- mice in 100% O2 was 101.4 ± 14.8 h (n = 20) versus 103.2 ± 11.3 h (n = 20) for Sod2+/+ littermates (P > 0.60). In addition, Sod2+/- mice with approximately 50% of normal heart MnSOD activity and Sod2+/+ mice did not develop any ultrastructural abnormalities in the myocardium at 75 h or 90 h after 100% O2 exposure. These results suggest that in mice, only 50% of MnSOD activity may be sufficient for normal resistance to 100% O2 toxicity.