Induction of arginase isoforms in the lung during hyperoxia

Loretta G. Que, Stephen P. Kantrow, Christopher P. Jenkinson, Claude A. Piantadosi, Yuh Chin T Huang

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Abstract

L-Arginine can be metabolized by nitric oxide (NO) synthase (NOS) to produce NO or by arginase to produce urea and L-ornithine. In the liver, arginase (the AI isoform) is a key enzyme in the urea cycle. In extrahepatic organs including the lung, the function of arginase (the AII isoform) is less clear. Because we found that lung AII was upregulated during 100% O2 exposure in preliminary experiments, we sought to characterize expression of the arginase isoforms and inducible NOS and to assess the functions of arginase in hyperoxic lung injury. Male Sprague-Dawley rats were exposed to 100% O2 for 60 h. Protein expression of AI and AII and their cellular distribution were determined. The activities of arginase and NOS were also measured. Expression of arginase was correlated with that of ornithine decarboxylase, a biochemical marker for tissue repair, in a separate group of rats allowed to recover in room air for 48 h. We found by Western blot analyses that both AI and AII proteins were upregulated after 60 h of hyperoxic exposure (403 and 88% increases by densitometry, respectively) and, like ornithine decarboxylase, remained elevated during the recovery phase. Arginase activity increased by 37%. Immunostaining showed that increases in AI and AII were mainly in the peribronchial and perivascular connective tissues. NOS activity was unchanged and inducible NOS was not induced, but the level of nitrogen oxides in the lung decreased by 67%. Our study showed in vivo induction of arginase isoforms during hyperoxia. The strong expression of arginase in the connective tissues suggests that the function of pulmonary arginase may be linked to connective tissue elements, e.g., fibroblasts, during lung injury and recovery.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume275
Issue number1 19-1
StatePublished - Jul 1998
Externally publishedYes

Fingerprint

Arginase
Hyperoxia
Protein Isoforms
Lung
Nitric Oxide Synthase
Connective Tissue
Ornithine Decarboxylase
Lung Injury
Urea
Nitrogen Oxides
Ornithine
Densitometry
Sprague Dawley Rats
Arginine
Nitric Oxide
Proteins
Fibroblasts
Biomarkers
Western Blotting
Air

Keywords

  • Nitric oxide
  • Nitric oxide synthase
  • Ornithine decarboxylase
  • Oxygen

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Que, L. G., Kantrow, S. P., Jenkinson, C. P., Piantadosi, C. A., & Huang, Y. C. T. (1998). Induction of arginase isoforms in the lung during hyperoxia. American Journal of Physiology - Lung Cellular and Molecular Physiology, 275(1 19-1).

Induction of arginase isoforms in the lung during hyperoxia. / Que, Loretta G.; Kantrow, Stephen P.; Jenkinson, Christopher P.; Piantadosi, Claude A.; Huang, Yuh Chin T.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 275, No. 1 19-1, 07.1998.

Research output: Contribution to journalArticle

Que, LG, Kantrow, SP, Jenkinson, CP, Piantadosi, CA & Huang, YCT 1998, 'Induction of arginase isoforms in the lung during hyperoxia', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 275, no. 1 19-1.
Que, Loretta G. ; Kantrow, Stephen P. ; Jenkinson, Christopher P. ; Piantadosi, Claude A. ; Huang, Yuh Chin T. / Induction of arginase isoforms in the lung during hyperoxia. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 1998 ; Vol. 275, No. 1 19-1.
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