Association between Glutathione and GSNO Reductase in Formaldehyde Inhaled Mice Lungs

Accumulating evidences demonstrate that the channeling of nitric oxide (NO) into S-nitrothiols (SNOs) plays a pivotal role in mediating NO actions. Recent work suggests that GSNO reductase (GSNOR), an enzyme responsible for SNO metabolism, is abnormally elevated under asthmatic conditions. To study GSNOR induction in mice lung, male Kun Ming mice were exposed to gaseous formaldehyde (FA) of 0, 3.0 mg/m³ and 3.0 mg/m³ with oc-lipoic acid (LA) injection, continuously for 3d. After exposure, GSNOR activity and transcription were examined, and GSH levels in broncho alveolar lavage fluid (BALF) were measured to indicate the oxidative stress. Results showed that GSNOR activity was elevated upon 3.0 mg/m³ FA exposure (compared with 0 mg/m³ FA inhaled group, p<0.01) and the elevation was completely inhibited by LA injection (compared with 3.0 mg/m³ FA inhaled group, p<0.01). Meanwhile, GSH levels were significantly decreased in 3.0 mg/m³ FA inhaled group (compared with 0 mg/m³ FA inhaled group, p<0.01), and were regenerated by LA injection (compared with 3.0 mg/m³ FA inhaled group, p<0.01). The expression of GSNOR correlated with the results of GSNOR activity assay. The results indicated that gaseous FA might activate GSNOR with the increase of oxidative stress. Since GSNOR has a central role in mediating SNO signaling and asthma development, these findings also suggested that indoor air pollutants such as FA might be key risk factors for the rise in asthma cases.