Generation of glycolaldehyde from guinea pig airway epithelial monolayers exposed to nitrogen dioxide and its effects on sodium pump activity.

Abstract

Pulmonary injury from nitrogen dioxide (NO2) may in part be related to the generation of aldehydic compounds, which bind with cellular proteins and subsequently impair or inhibit cell function. We examined the generation of aldehydes from guinea pig tracheobronchial epithelial (GPTE) cell monolayers exposed to NO2. With the use of dinitrophenylhydrazine (DNP) to derivatize aldehydic compounds, glycolaldehyde, a two carbon alpha-hydroxyaldehyde, was identified in elevated levels in the basolateral fluid from monolayers exposed to NO2. DNP-glycolaldehyde levels were 81.2 +/- 2.7 and 234.0 +/- 42.6 nM in response to a 1-hr exposure to 1 and 5 ppm NO2, respectively, as compared to an air-control value 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 exogenous glycolaldehyde on GPTE ouabain-sensitive basolateral 86Rb uptake (an index of Na+,K(+)-ATPase activity) were examined and compared with the actions of NO2 exposure. Bolus addition of glycolaldehyde to the basolateral fluid at concentrations > or = 5 mM led to an inhibition of ouabain-sensitive 86Rb uptake, while lower concentrations had no effect. the effects of exogenous glycolaldehyde differ from NO2 exposure, which led to a sustained elevation of ouabain-sensitive 86Rb uptake with presumed generation of glycolaldehyde at a continuous low level. Glycolaldehyde does not appear to play a significant role in the acute alterations of sodium pump activity, suggesting that the NO2-induced changes in Na+,K(+)-ATPase activity of GPTE monolayers probably are further mediated by other lipid peroxidation products/oxidation processes yet to be identified. Images Figure 1. Figure 2. Figure 3. Figure 4.

Glycolaldehyde, a reactive intermediate for advanced glycation end products, plays an important role in the generation of an active ligand for the macrophage scavenger receptor.

“…Therefore, it seems likely that GA, glyoxal, and methylglyoxal could contribute, as intermediates, to AGE structures generated in glucose-derived AGE proteins in vitro. Furthermore, in vivo presence of these aldehydes is also supported by data from several studies (19,(24)(25)(26)(27). For example, in addition to GA derived from the Maillard reaction, the myeloperoxidase pathway has been reported.…”

Profile of Patients with Chemical Injury and Sensitivity, Part II

“…A higher level of autoantibodies are described after a wide variety of chemical exposures, including chlordane (Robinson 1996), solvents (Daniell, Couser, and Rosenstock 1988;Bombassei and Kaplan 1992), chlorinated solvents (Montoya 1990), PCBs/PBBs (Safran et al 1987), organochlorine, organophosphate and other pesticides (Street 1981), formaldehyde and aliphatic amines (Brooks et al 1985), silicone (Press et al 1992;, chlordane (Ziem and McTamney 1997), chlorpyrifos (Ziem and McTamney 1997), malathion (Ziem and McTamney 1997), and formaldehyde (Tarlo and Broder 1989). A greater number of chemical-speci c antibodies has been noted after exposure to building materials in remodeling (Thrasher et al 1989).…”

“…It has long been known that overexposure to petrochemicals can induce fatigue. Petrochemicals generate free radicals which can damage energy metabolism, causing fatigue (Robinson 1996). Petrochemical damage to nerves can result in muscle fatigue during nerve regeneration (Anderson 1992).…”