Survival, lung injury, and lung protein nitration in heterozygous MnSOD knockout mice in hyperoxia

Robert M. Jackson, Eric S. Helton, Liliana Viera, Tauni Ohman

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


This study tested whether a strain of heterozygous Mn superoxide dismutase (SOD) knockout mice differed from wild types in response to lethal (100 or 85%) or sublethal (50 or 75%) oxygen exposures. Lung MnSOD activity was significantly (-40%) less in the heterozygous mice, and lung catalase activity was also significantly decreased. Total SOD activity, glutathione peroxidase, and glutathione reductase did not differ between heterozygous (+/-) and wild-type (+/+) mice. We exposed both heterozygous and wild-type mice to hyperoxia (50, 75, 85, or 100% oxygen) until death or for 48 hours to assess sublethal lung injury. Survival of the heterozygous and wild-type mice did not differ significantly in 100 or 85% oxygen. No mice of either genotype died in 50 or 75% oxygen (14-day exposures). Hyperoxia exposures significantly increased (by two-way ANOVA) the alveolar lavage protein concentration, percent neutrophils, and lung wet-dry/dry weight ratios. No significant differences occurred between the heterozygous and wild-type mice for any marker of injury at any oxygen level. Lavage fluid total nitrite concentrations did not differ at any oxygen level. Hyperoxia caused a similar degree of nitration of lung structural proteins detected by immunohistochemistry in both groups.

Original languageEnglish (US)
Pages (from-to)631-646
Number of pages16
JournalExperimental Lung Research
Issue number7
StatePublished - Nov 17 1999
Externally publishedYes


  • Hyperoxia
  • Lung injury
  • Mice
  • Mitochondria
  • Superoxide dismutase

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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