Background: Reactive nitrogen, oxygen species and oxidative stress are related to many pulmonary diseases. Nitric oxide (NO) may be involved in either the protection against or the induction of oxidative stress within various tissues. It is derived from the amino acid L-arginine by the action of NO synthase (NOS). L-arginine can also be metabolized by arginase with the production of ornithine and urea. Because of the competition between NOS and arginase for the same substrate, their activities are regulated reciprocally. Therefore, the rate of NO generation associated with oxidative stress is dependent on the relative activities of both NOS and arginase. The objective of this study is to investigate the L-arginine-NO pathway, evaluate oxidative-antioxidative status in the patients with asthma and demonstrate their reciprocal regulation.