Evaluation of oxidative-antioxidative status and the L-arginine-nitric oxide pathway in asthmatic patients

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.

30 voluntary asthmatic patients and 30 healthy control subjects with similar age range and sex were included in the study. A total of 10 ml venous blood was drawn, plasma and packed erythrocytes were prepared for the biochemical analyses. Plasma arginase activities and NO levels, and erythrocyte malondialdehyde and reduced glutathione levels were detected.

Plasma malondialdehyde levels were significantly higher and glutathione levels were lower in patients with asthma than those of the control subjects (P < 0.001 and P < 0.01, respectively). Arginase activities were significantly lower and NO levels were higher in the patients than those of the controls (P < 0.001 for both). The negative correlation between arginase and NO levels in the patients was significant (r = -0.47; P < 0.01). There was also a positive correlation between malondialdehyde and NO levels in the patients (r = 0.51; P < 0.01).

The results suggest that the L-arginine-NO pathway is involved in the pathophysiology of asthma; the arginase activities decrease which causes an increase in the L-arginine levels thereby up-regulation of NO production may contribute to the increase of oxidative stress in asthma.