Abstract
Recent work showed that GSNO reductase (GSNOR) mediates the equilibrium of nitric oxide (NO) and the adduct molecules, S-nitrosothiols (SNOs) in lungs of asthmatic mice, and thus, plays a central role in the physiology and patho-physiology in lung diseases. To further understand the role of GSNOR in mediating asthma development, it is essential to examine the possible factors that can activate GSNOR in lungs. In present study, male Kun Ming mice were divided into 3 testing groups (n=6 each) and inhaled with formaldehyde (FA) of 0, 1.0, 3.0 mg/m3 continuously for 72h, 3d, respectively. Immediately after exposure, GSNOR RT-PCR and enzyme activity assay were performed in lungs of mice. Results showed that GSNOR is expressed in lungs of mice, and GSNOR expression was significantly up regulated in lungs of 3.0 mg/m3 FA inhaled group (compared with 0 mg/m3 FA inhaled group, p<0.05). Consistent with RT-PCR results, enzyme activity assay showed that GSNOR activity increased in a dose-dependent manner, and the reductase activity increased significantly in lungs both of 1.0 mg/m3 and 3.0 mg/m3 FA inhaled group (compared with 0 mg/m3 FA inhaled group, p<0.01). The results indicated that gaseous FA could activate GSNOR in lungs. These findings also suggested that small metabolic substrates of GSNOR like FA could activate GSNOR and might be key risk factors for the rise in asthma cases.
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