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Induction of arginase isoforms in the lung during hyperoxia.

Publication ,  Journal Article
Que, LG; Kantrow, SP; Jenkinson, CP; Piantadosi, CA; Huang, YC
Published in: Am J Physiol
July 1998

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.

Duke Scholars

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

July 1998

Volume

275

Issue

1

Start / End Page

L96 / 102

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Nitrogen Oxides
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Male
  • Lung
  • Isoenzymes
  • Immunohistochemistry
  • Hyperoxia
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Que, L. G., Kantrow, S. P., Jenkinson, C. P., Piantadosi, C. A., & Huang, Y. C. (1998). Induction of arginase isoforms in the lung during hyperoxia. Am J Physiol, 275(1), L96-102. https://doi.org/10.1152/ajplung.1998.275.1.L96
Que, L. G., S. P. Kantrow, C. P. Jenkinson, C. A. Piantadosi, and Y. C. Huang. “Induction of arginase isoforms in the lung during hyperoxia.Am J Physiol 275, no. 1 (July 1998): L96-102. https://doi.org/10.1152/ajplung.1998.275.1.L96.
Que LG, Kantrow SP, Jenkinson CP, Piantadosi CA, Huang YC. Induction of arginase isoforms in the lung during hyperoxia. Am J Physiol. 1998 Jul;275(1):L96-102.
Que, L. G., et al. “Induction of arginase isoforms in the lung during hyperoxia.Am J Physiol, vol. 275, no. 1, July 1998, pp. L96-102. Pubmed, doi:10.1152/ajplung.1998.275.1.L96.
Que LG, Kantrow SP, Jenkinson CP, Piantadosi CA, Huang YC. Induction of arginase isoforms in the lung during hyperoxia. Am J Physiol. 1998 Jul;275(1):L96-102.

Published In

Am J Physiol

DOI

ISSN

0002-9513

Publication Date

July 1998

Volume

275

Issue

1

Start / End Page

L96 / 102

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Nitrogen Oxides
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase
  • Male
  • Lung
  • Isoenzymes
  • Immunohistochemistry
  • Hyperoxia