Manganese superoxide dismutase expression in alveolar type II epithelial cells from nonventilated and hypoperfused lungs.

W. J. Russell, S. Matalon, Robert Jackson

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Abstract

Lungs that have been hypoxic and hypoperfused because of atelectasis and the resulting decrease in pulmonary arterial blood flow develop specific decreases in manganese superoxide dismutase (MnSOD) activity and are sensitive to oxidant injury during reoxygenation. Since the MnSOD protein is concentrated in mitochondria of alveolar epithelial type II cells (ATII), we hypothesized that expression of MnSOD would be decreased in these cells also as a result of hypoxia. To investigate whether regulation of MnSOD expression occurred before or after transcription, we determined whether MnSOD protein content or steady-state mRNA level changed after hypoxia as well. ATII cells were isolated by elastase digestion from lungs of adult rabbits after right lungs had been hypoxic and hypoperfused for 7 days because of unilateral atelectasis. MnSOD activity was measured by inhibition of cytochrome c reduction in the presence of 1 mM KCN, MnSOD protein content was measured on immunoblots, and MnSOD mRNA was quantified on slot blot autoradiograms. MnSOD activity was 8.4 +/- 1.9 U/mg protein in ATII cells from control lungs and 6.8 +/- 1.5 U/mg protein in ATII cells from hypoxic and hypoperfused lungs (n = 9, P = 0.037). MnSOD protein content was 5.1 +/- 1.4 micrograms/mg protein in ATII cells from control and 4.1 +/- 1.2 micrograms/mg protein in ATII cells from hypoxic and hypoperfused lungs (P = 0.021). ATII cell MnSOD mRNA/18S ribosomal RNA (ratio of arbitrary absorbance units) determined by RNA slot blots was 2.18 +/- 1.26 in ATII cells from control lungs and 2.94 +/- 0.88 in ATII cells from hypoxic lungs (n = 7, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Original languageEnglish
Pages (from-to)366-371
Number of pages6
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume11
Issue number3
StatePublished - Sep 1 1994
Externally publishedYes

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Alveolar Epithelial Cells
Superoxide Dismutase
Lung
Proteins
Pulmonary Atelectasis
Messenger RNA
Epithelial Cells
18S Ribosomal RNA
Mitochondria
Pancreatic Elastase
Transcription
Cytochromes c
Oxidants
Digestion
Blood

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Pulmonary and Respiratory Medicine

Cite this

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abstract = "Lungs that have been hypoxic and hypoperfused because of atelectasis and the resulting decrease in pulmonary arterial blood flow develop specific decreases in manganese superoxide dismutase (MnSOD) activity and are sensitive to oxidant injury during reoxygenation. Since the MnSOD protein is concentrated in mitochondria of alveolar epithelial type II cells (ATII), we hypothesized that expression of MnSOD would be decreased in these cells also as a result of hypoxia. To investigate whether regulation of MnSOD expression occurred before or after transcription, we determined whether MnSOD protein content or steady-state mRNA level changed after hypoxia as well. ATII cells were isolated by elastase digestion from lungs of adult rabbits after right lungs had been hypoxic and hypoperfused for 7 days because of unilateral atelectasis. MnSOD activity was measured by inhibition of cytochrome c reduction in the presence of 1 mM KCN, MnSOD protein content was measured on immunoblots, and MnSOD mRNA was quantified on slot blot autoradiograms. MnSOD activity was 8.4 +/- 1.9 U/mg protein in ATII cells from control lungs and 6.8 +/- 1.5 U/mg protein in ATII cells from hypoxic and hypoperfused lungs (n = 9, P = 0.037). MnSOD protein content was 5.1 +/- 1.4 micrograms/mg protein in ATII cells from control and 4.1 +/- 1.2 micrograms/mg protein in ATII cells from hypoxic and hypoperfused lungs (P = 0.021). ATII cell MnSOD mRNA/18S ribosomal RNA (ratio of arbitrary absorbance units) determined by RNA slot blots was 2.18 +/- 1.26 in ATII cells from control lungs and 2.94 +/- 0.88 in ATII cells from hypoxic lungs (n = 7, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)",
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N2 - Lungs that have been hypoxic and hypoperfused because of atelectasis and the resulting decrease in pulmonary arterial blood flow develop specific decreases in manganese superoxide dismutase (MnSOD) activity and are sensitive to oxidant injury during reoxygenation. Since the MnSOD protein is concentrated in mitochondria of alveolar epithelial type II cells (ATII), we hypothesized that expression of MnSOD would be decreased in these cells also as a result of hypoxia. To investigate whether regulation of MnSOD expression occurred before or after transcription, we determined whether MnSOD protein content or steady-state mRNA level changed after hypoxia as well. ATII cells were isolated by elastase digestion from lungs of adult rabbits after right lungs had been hypoxic and hypoperfused for 7 days because of unilateral atelectasis. MnSOD activity was measured by inhibition of cytochrome c reduction in the presence of 1 mM KCN, MnSOD protein content was measured on immunoblots, and MnSOD mRNA was quantified on slot blot autoradiograms. MnSOD activity was 8.4 +/- 1.9 U/mg protein in ATII cells from control lungs and 6.8 +/- 1.5 U/mg protein in ATII cells from hypoxic and hypoperfused lungs (n = 9, P = 0.037). MnSOD protein content was 5.1 +/- 1.4 micrograms/mg protein in ATII cells from control and 4.1 +/- 1.2 micrograms/mg protein in ATII cells from hypoxic and hypoperfused lungs (P = 0.021). ATII cell MnSOD mRNA/18S ribosomal RNA (ratio of arbitrary absorbance units) determined by RNA slot blots was 2.18 +/- 1.26 in ATII cells from control lungs and 2.94 +/- 0.88 in ATII cells from hypoxic lungs (n = 7, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

AB - Lungs that have been hypoxic and hypoperfused because of atelectasis and the resulting decrease in pulmonary arterial blood flow develop specific decreases in manganese superoxide dismutase (MnSOD) activity and are sensitive to oxidant injury during reoxygenation. Since the MnSOD protein is concentrated in mitochondria of alveolar epithelial type II cells (ATII), we hypothesized that expression of MnSOD would be decreased in these cells also as a result of hypoxia. To investigate whether regulation of MnSOD expression occurred before or after transcription, we determined whether MnSOD protein content or steady-state mRNA level changed after hypoxia as well. ATII cells were isolated by elastase digestion from lungs of adult rabbits after right lungs had been hypoxic and hypoperfused for 7 days because of unilateral atelectasis. MnSOD activity was measured by inhibition of cytochrome c reduction in the presence of 1 mM KCN, MnSOD protein content was measured on immunoblots, and MnSOD mRNA was quantified on slot blot autoradiograms. MnSOD activity was 8.4 +/- 1.9 U/mg protein in ATII cells from control lungs and 6.8 +/- 1.5 U/mg protein in ATII cells from hypoxic and hypoperfused lungs (n = 9, P = 0.037). MnSOD protein content was 5.1 +/- 1.4 micrograms/mg protein in ATII cells from control and 4.1 +/- 1.2 micrograms/mg protein in ATII cells from hypoxic and hypoperfused lungs (P = 0.021). ATII cell MnSOD mRNA/18S ribosomal RNA (ratio of arbitrary absorbance units) determined by RNA slot blots was 2.18 +/- 1.26 in ATII cells from control lungs and 2.94 +/- 0.88 in ATII cells from hypoxic lungs (n = 7, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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