| First Author | Jackson RM | Year | 1999 |
| Journal | Exp Lung Res | Volume | 25 |
| Issue | 7 | Pages | 631-46 |
| PubMed ID | 10598322 | Mgi Jnum | J:103295 |
| Mgi Id | MGI:3609094 | Doi | 10.1080/019021499270060 |
| Citation | Jackson RM, et al. (1999) Survival, lung injury, and lung protein nitration in heterozygous MnSOD knockout mice in hyperoxia. Exp Lung Res 25(7):631-46 |
| abstractText | 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. |
