Arginine is a conditionally essential amino acid. Sufficient arginine may not be available in asthma due to an imbalance between the nitric oxide synthase (NOS) and the arginase enzymes. A deficiency of arginine may cause the airway the hyperresponsiveness (AHR) seen in asthma. The arginase enzyme is increased in asthma.
Nitric oxide (NO) is produced by the NOS enzyme. The rate limiting factor on NO production is sufficient arginine. Previous studies have used 50 mg/kg of arginine. This dose may be too low. This study used the high dose of 250 mg/kg. The goal of this study was to evaluate the effects of high doses of arginine, including airway hyperresponsiveness (AHR.) (L-arginine has been used at a dose of 30 gm/day without toxic effects.)
Peroxynitrite is produced by NOS when arginine is insufficient. It causes bronchoconstriction and inflammation of the airways. Oxidative stress and mitochondrial dysfunction are seen in allergic airway inflammation (AAI.) Increased NO is exhaled by people with AAI. But, blocking NOS does not improve asthma.
Mice were tested with various doses of arginine and testing was done of the enzymes in lung tissue. The administration of arginine significantly reduced AHR, increased NOS and reduced inflammation. Arginine significantly reduced the amount of thick collagen that develops in the bronchovascular region in allergies. Arginase is increased in AAI in lung tissue.
Testing of animals with arginase inhibitors has shown some benefit to AHR. Treatment with l-arginine reduced the amount of arginase and reduced the inflammation. Long term treatment with arginine may have some side effects of causing structural changes in airways and prolonging the treatments.
CONCLUSION: Arginine improves some symptoms of asthma and improves NO metabolism and allergic airway inflammation (AAI.) Arginine reduces symptoms of asthma at a dose of 250 mg/kg. Arginase inhibitors are beneficial in animal studies.
NOTE: Read about the benefit of arginase inhibitors in arginine therapy.
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