L-arginine is metabolized by the arginase enzyme and by the nitric oxide synthase (NOS) enzyme. Abnormalities in the arginine and the arginase and nitric oxide synthase pathways can lead to airway hyperresponsiveness (AHR,) as seen in asthma. Exhaled levels of nitric oxide (NO) are elevated in asthma. Arginine therapy has been shown to be beneficial in asthma.

Arginase enzyme maintains high airway tone by reducing the amount of arginine available to NOS to produce NO. NO would relax the airways. The author’s purpose was to study further the role of arginase enzymes in AHR.

The authors found that there was increased expression of the arginase enzyme in tissues from lung samples from humans with asthma. These were compared to normal control patients who did not have asthma. Most arginine related proteins were unchanged. There is research evidence in support of the theory that there is competition for arginine in allergic asthma by arginase and NOS.

In the animal model of asthma, arginase inhibition resulted in reduced AHR. The present study shows the potential benefit of arginase inhibition in the treatment of asthma. Chronic models of asthma in animals show evidence for long term changes in the airways, which prolong the need for treatment.

Some studies have shown reduced availability of l-arginine in pediatric asthma.

CONCLUSION: Therapeutic roles are seen for arginine and arginase inhibitors in asthma. Specifically, inhibitors of arginase-1 should be of benefit. More studies need to be done.

NOTE: The arginase enzyme acts on arginine to produce ornithine and urea. The nitric oxide synthase enzyme acts on arginine to produce nitric oxide, citrulline and peroxynitrite.

L-arginine is the natural form of arginine amino acid. Read more about the effect of arginine in the airways in asthma.

To read the author’s abstract of the article click on the link to the author’s title of the article above.

PMID: 19286931.

Summary #413.