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Induction of arginase isoforms in the lung during hyperoxia

L G Que1, S P Kantrow, C P Jenkinson

  • 1Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.

The American Journal of Physiology
|August 5, 1998
PubMed
Summary

This study shows that arginase, an enzyme involved in L-ornithine production, is upregulated in the lungs during hyperoxic lung injury and recovery. This suggests arginase plays a role in lung repair processes.

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Area of Science:

  • Biochemistry
  • Pulmonary Medicine
  • Cellular Biology

Background:

  • L-arginine metabolism involves nitric oxide (NO) synthase (NOS) and arginase, producing NO or L-ornithine and urea, respectively.
  • Arginase isoform AI is crucial in the liver's urea cycle, while the function of the AII isoform in extrahepatic organs like the lung is less understood.
  • Preliminary findings indicated upregulation of lung arginase AII during hyperoxia, prompting further investigation.

Purpose of the Study:

  • To characterize the expression of arginase isoforms (AI and AII) and inducible NOS in the lung during hyperoxic lung injury.
  • To assess the functional role of arginase in hyperoxic lung injury and subsequent recovery.
  • To investigate the correlation between arginase expression and ornithine decarboxylase, a marker of tissue repair.

Main Methods:

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  • Male Sprague-Dawley rats were exposed to 100% oxygen (hyperoxia) for 60 hours.
  • Western blot analysis was used to determine protein expression and cellular distribution of arginase isoforms AI and AII.
  • Arginase and NOS activities were measured, and immunostaining was performed. Ornithine decarboxylase expression was assessed during a recovery phase.

Main Results:

  • Both arginase isoforms (AI and AII) protein levels significantly increased (403% and 88%, respectively) after 60 hours of hyperoxia and remained elevated during recovery.
  • Arginase activity increased by 37%, while NOS activity remained unchanged and inducible NOS was not detected.
  • Increased arginase expression was localized to peribronchial and perivascular connective tissues, and correlated with ornithine decarboxylase levels during recovery.

Conclusions:

  • Hyperoxia induces arginase isoforms in the lung in vivo.
  • The localization of arginase in connective tissues suggests a role in lung injury and repair, potentially involving fibroblasts.
  • Arginase may play a significant role in the lung's response to hyperoxic injury and the subsequent tissue repair processes.