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EPO and MPO are increased in the peripheral blood, induced sputum, and BAL fluid of patients with asthma.65–68 Many direct or indirect markers of oxidative stress, including malondialdehyde, thiobarbituric acid, and glutathione disulfide, have been found in urine, plasma, sputum, and BAL fluid of patients with asthma, and the level of the markers correlated with the severity of the disease.67–69 Analysis of exhaled breath condensate has allowed direct measurements of H 2 O 2 and NO and the measurement of several indirect by-products of oxidation like isoprostane and ethane.20,21 Despite the difficulties to quantify the ROS because of their labile nature, the stable end products of the reactive pathways may be used as reliable markers of oxidative stress in patients with asthma.7 One clinically useful biomarker of airway inflammation is exhaled NO.7 During an asthma exacerbation and in the case of uncontrolled asthma, the airway environment becomes more acidic and oxidizing that leads to the release of NO from S-nitrosoglutathione (GSN), which leads to high levels of exhaled NO.2 FUTURE PERSPECTIVES FOR ANTI-OXIDANT TREATMENT Even though it is apparent that treatment modalities targeting the oxidant stress has a great potential for the treatment of many diseases including asthma, so far, human studies have failed to reveal a clear benefit