{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T00:43:08Z","timestamp":1772930588925,"version":"3.50.1"},"reference-count":24,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[1998,7,1]],"date-time":"1998-07-01T00:00:00Z","timestamp":899251200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1998,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Recent studies have shown that homozygous Mn superoxide dismutase (Sod2) gene-knockout mice (Sod2\u2212\/\u2212) die shortly after birth with extensive myocardial injury, whereas heterozygous mutants (Sod2+\/\u2212) are phenotypically normal in room air. In the current study, we showed that Sod2+\/\u2212 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 (\u00b1 SD) survival of Sod2+\/\u2212 mice in 100% O2 was 101.4 \u00b1 14.8 h (n = 20) versus 103.2 \u00b1 11.3 h (n = 20) for Sod2+\/+ littermates (P &amp;gt; 0.60). In addition, Sod2+\/\u2212 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.<\/jats:p>","DOI":"10.1165\/ajrcmb.19.1.3066","type":"journal-article","created":{"date-parts":[[2013,4,3]],"date-time":"2013-04-03T22:15:05Z","timestamp":1365027305000},"page":"114-120","source":"Crossref","is-referenced-by-count":60,"title":["Susceptibility of Heterozygous MnSOD Gene-Knockout Mice to Oxygen Toxicity"],"prefix":"10.1093","volume":"19","author":[{"given":"Min-Fu","family":"Tsan","sequence":"first","affiliation":[{"name":"Research and Laboratory Services, Samuel S. Stratton Department of Veterans Affairs Medical Center; Departments of Physiology, Medicine, Pathology, and Laboratory Medicine, Albany Medical College, Albany, New York; and Department of Pediatrics, University of California, San Francisco, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie E.","family":"White","sequence":"additional","affiliation":[{"name":"Research and Laboratory Services, Samuel S. Stratton Department of Veterans Affairs Medical Center; Departments of Physiology, Medicine, Pathology, and Laboratory Medicine, Albany Medical College, Albany, New York; and Department of Pediatrics, University of California, San Francisco, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbara","family":"Caska","sequence":"additional","affiliation":[{"name":"Research and Laboratory Services, Samuel S. Stratton Department of Veterans Affairs Medical Center; Departments of Physiology, Medicine, Pathology, and Laboratory Medicine, Albany Medical College, Albany, New York; and Department of Pediatrics, University of California, San Francisco, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charles J.","family":"Epstein","sequence":"additional","affiliation":[{"name":"Research and Laboratory Services, Samuel S. Stratton Department of Veterans Affairs Medical Center; Departments of Physiology, Medicine, Pathology, and Laboratory Medicine, Albany Medical College, Albany, New York; and Department of Pediatrics, University of California, San Francisco, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. Y.","family":"Lee","sequence":"additional","affiliation":[{"name":"Research and Laboratory Services, Samuel S. 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