GENERATION OF GLYCOLALDEHYDE FROM GUINEA-PIG AIRWAY EPITHELIAL MONOLAYERS EXPOSED TO NITROGEN-DIOXIDE AND ITS EFFECT ON SODIUM-PUMP ACTIVITY

Pulmonary injury from nitrogen dioxide (NO2) may in part be related to the generation of aldehydic compounds, which bind with cellular prote ins and subsequently impair or inhibit cell unction Vee examined the g eneration of aldehydes from guinea pig tracheobronchial epithelial (GP TE) cell monolayers exposed to NO2. With the use of dinitrophenylhydra zine (DNP) to derivatize aldehydic compounds, glycolaldehyde, a two ca rbon alpha-hydroxy aldehyde, was identified in elevated levels in the basolateral fluid from monolayers exposed to NO2.DNP-glycoladehyde lev els were 81.2 +/- 2.7 and 234.0 +/- 42.6 nM in response to a 1-hr expo sure to 1 and 5 ppm NO2, respectively, as compared to an air-control v alue of 20.3 +/- 6.8 nM. Taking into account dilution and reactivity, cellular glycolaldehyde levels could have reached as high as 3 mM for the 60-min exposure period (i.e., 0.05 mM/min). The effects of exogeno us glycolaldehyde on GPTE onabain-sensitive basolateral Rb-86 uptake ( an index of Na+,K+-ATPase activity) were examined and compared with th e actions of NO2 exposure. Bolus addition of glycolaldehyde to the bas olateral fluid at concentrations greater than or equal to 5 mM led to an inhibition of ouabain-sensitive Rb-86 uptake, lower concentrations had no effect. The effects of exogenous glycolaldehyde differ from NO2 exposure, which led to a sustained elevation of ouabain-sensitive Rb- 86 uptake with presumed generation of glycolaldehyde at a continuous l ow level. Glycolaldehyde does not appear to a significant role in the acute alterations of sodium pump activity, suggesting that the NO2- ch anges in Na+,K+-ATPase activity of GPTE monolayers probably are furthe r mediated by other lipid peroxidation products/oxidation processes ye t to be identified.