Arginine and asthma.

摘要: Recent studies suggest that alterations of the arginine metabolome and a dysregulation nitric oxide (NO) homeostasis play role in pathogenesis asthma. L-Arginine, semi-essential amino acid, is common substrate for both arginases NO synthase (NOS) enzyme families. an important vasodilator bronchial circulation, with bronchodilatory anti-inflammatory properties, synthesized from oxidation its obligate L-arginine, which catalyzed by family NOS enzymes. Arginase essential urea cycle, responsible conversion to ornithine urea. The arginase enzymes can be expressed simultaneously under wide variety inflammatory conditions, resulting competition their substrate. Although much attention has been directed towards measurements exhaled asthma, accumulating data show low bioavailability L-arginine also contributes inflammation, hyperresponsiveness remodeling asthmatic airway. Aberrant catabolism represents novel asthma paradigm involves excess activity, elevated levels asymmetric dimethyl arginine, altered intracellular transport, dysfunction. Addressing metabolism may result new strategies treatment