Thione levels in the exhaled breath condensate of children were found to be lower than

May 28, 2018

Thione levels in the exhaled breath condensate of children were found to be lower than those in the control subjects. In addition, the glutathione levels in exhaled breath condensate increased after oral steroid treatment compared with pretreatment levels.55 Glutathione depletion leads to the inhibition of Th1-associated cytokine production and favors Th2-associated response.56 In other words, reduction in glutathione levels supports the maintenance of Th2 response in asthma.GENES AND AZD-8835 cost oxidative STRESS IN ASTHMAGlutathione S-transferases (GST) include a number of subclasses, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28128382 such as GST-P1 and GST-M1, that are expressed in the lungs and have been implicated in the pathogenesis of asthma. Children with GSTM1 null or GSTP1 val/val genotypes had increased respiratory symptoms upon exposure to ozone.33,57,58 The same genotypes were associated with higher nasal IgE and histamine response.59 Because theseSahiner et alWAO Journal Octoberpolymorphisms have a high frequency,60 they may have a substantial effect at the population level. GSTCD gene at 4q24 location was identified as one of the primary genes that determine lung function.61 We genotyped patients with asthma and healthy individuals for null variants of GSTT1 and GSTM1 and ile105val variant of GSTP1. Children with asthma possessing the GSTP1 val/val genotype had higher malondialdehyde and lower glutathione levels compared with other genotypes in the systemic circulation but not in the airways.33,62 This particular genotype was independently associated with the severity of childhood asthma. Similar genetic effects have been reported for SOD. Ala16Val mutation in Mn-SOD changes the secondary structure of the protein, which may affect the targeting of the protein to mitochondria.63 The EC-SOD R213G polymorphism is associated with reduced exacerbations in chronic obstructive pulmonary disease (COPD) and lower rates of hospitalization.64 However, neither R213G (EC-SOD) nor Ala16Val of Mn-SOD was associated with a genetic susceptibility to develop asthma.63 This is an area that needs further research (Fig. 3).and the level of the markers correlated with the severity of the disease.67?9 Analysis of exhaled breath condensate has allowed direct measurements of H2O2 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.FUTURE PERSPECTIVES FOR ANTI-OXIDANT TREATMENTEven 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.CLINICAL MONITORING OF OXIDATIVE STRESS IN ASTHMAOxidants are produced at higher amounts either spontaneously or after the stimulation in patients with asthma compared with healthy subjects. EPO and MPO are increased in the peripheral blood, induced sputum, and BAL fluid of patients with asthma.65?8 Many direct or indirect markers of oxidative stress, including malondialde.