Allergic asthma causes obstruction of bronchi and airway hyperresponiveness (AHR.) Eventually, there are inflammation and remodeling of the airways. The enzyme, arginase, may play a part in this. Reduced availability of arginine may be involved, resulting in problems with bronchoconstriction from reduced levels of nitric oxide (NO.) Arginine deficiency results in increased levels of peroxynitrite, which increases bronchoconstriction and inflammation.
Because of increased amounts of ornithine, the increased arginase activity may be responsible for collagen deposition and the airway remodeling seen in chronic asthma. Arginase is necessary for removal of the toxic ammonium from the body. Arginase converts arginine to ornithine and urea. Nitric oxide (NO) synthase converts arginine to citrulline and NO. These two reactions compete for the available arginine. The balance is delicate.
NO, produced by nitric oxide synthase, is a bronchodilator which causes smooth muscle relaxation. NO exhalation is increased in breath of asthmatics after treatment with l-arginine.
More ornithine increases the production of proline and polyamines, such as putrescine, spermidine and spermine, and collagen in asthma. Polyamines increase the production of genes involved in cell reproduction. Collagen leads to airway fiber formation in chronic asthma. Airway remodeling results from chronic inflammation of asthma. There are structural changes in the airways which result in reduced lung function and persistent AHR.
Arginase inhibitors are suggested to increase the production of reduce inflammatory production and to prevent collagen production.
CONCLUSION: The increased arginase activity seen in asthma may be the cause of airway obstruction, with reduced arginine being available to NOS enzymes for the production of bronchial relaxing NO. Arginase inhibitors may be useful in acute and chronic asthma by increasing the arginine available for NO production.
Read about rhubarb as an arginase inhibitor.
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