Role of oxidative stress and FAS-induced apoptosis in acute lung injury

The purpose of our research was to study the FAS/FASL system in acute lung injury (ALI) (acute respiratory distress syndrome [ARDS]) and to compare these processes with dynamics of oxidative stress markers (nitric oxide [NO], hydrogen peroxide [H₂O₂]).

We examined expired air condensates (EAC) of patients with various stages of ARDS using spectrophotometry to study NO metabolites and fluorescence to study H₂O₂. Identification of CD95 (FAS) in blood cells was detected using monoclonal antibodies.

Our investigation showed the increase of NO metabolite level in EAC patients with the first and second stages of ARDS and its significant decrease in EAC patients with the third and fourth stages. The level of H₂O₂ in EAC elevated with the progress of ARDS. All these patients have increased FASL production, but we noted a reduction of the CD95 level in patients with the final ARDS stage.

These data show that alveolar epithelial injury in ALI or ARDS is in part associated with upregulation of the FAS/FASL system and activation of oxidative stress markers. Our findings suggest that oxygen-independent pathways may mainly operate in the process of FAS-induced apoptosis.