Effects of hypoxia on MnSOD expression in mouse lung

W. J. Russell, Y. S. Ho, G. Parish, R. M. Jackson

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

Mitochondrial manganese-containing SOD (MnSOD) is located at the primary site of O2 metabolism, and its expression may be regulated by changes in O2 level. We hypothesised that lung MnSOD expression and promoter activity would decrease in response to hypoxia. We tested effects of hypoxia (10% O2 at sea level for 7 days) on chloramphenicol acetyltransferase (CAT) reporter and MnSOD gene expression in transgenic mice. The transgene consisted of a 3.3- kb portion of the rat MnSOD gene 5' flanking region coupled to a CAT reporter gene. Lung MnSOD activity in male (but not female) mice decreased significantly after hypoxia exposure. The decrease in MnSOD enzymatic activity in male mice was specific. Neither total SOD nor glucose-6-phosphate dehydrogenase (G-6-PDH) activity decreased significantly in hypoxia. CAT protein expression decreased in transgenic males exposed to hypoxia, while CAT protein expression in hypoxic transgenic females remained comparable with controls. The mRNA for both the native MnSOD and the MnSOD-CAT reporter genes remained constant after hypoxia, as did CuZnSOD and G-6-PDH mRNAs.

Original languageEnglish (US)
Pages (from-to)L221-L226
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume269
Issue number2 13-2
DOIs
StatePublished - 1995
Externally publishedYes

Keywords

  • gene regulation
  • oxygen toxicity
  • superoxide dismutase

ASJC Scopus subject areas

  • Cell Biology
  • Physiology
  • Pulmonary and Respiratory Medicine

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