| First Author | Tsan MF | Year | 1998 |
| Journal | Am J Respir Cell Mol Biol | Volume | 19 |
| Issue | 1 | Pages | 114-20 |
| PubMed ID | 9651187 | Mgi Jnum | J:114195 |
| Mgi Id | MGI:3688482 | Doi | 10.1165/ajrcmb.19.1.3066 |
| Citation | Tsan MF, et al. (1998) Susceptibility of heterozygous MnSOD gene-knockout mice to oxygen toxicity. Am J Respir Cell Mol Biol 19(1):114-20 |
| abstractText | 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. |
