Introduction: Experimental models of acute lung injury treated with PFOB exhibit attenuation in tissue damage and inflammation. We have previously demonstrated an attenuation in oxidative injury to the lung in animals treated with PLV1. Since oxidative damage to tissues is preceded by the generation of reactive oxygen species, and peroxyl radicals cause oxidative injury, we hypothesized that PFOB might attenuate oxidative injury by acting as a scavenger for peroxyl radicals. Methods: We studied the in vitro peroxidation of alkali-activated dihydrochloro-fluorescein diacetate (DCFH-DA, 160 mM) in the absence (control, n=4) or presence of PFOB (PFOB, n=4). Various concentrations (25-50 mM) of AAPH, an azo-compound that generates peroxyl radicals during thermal decomposition, were used as the peroxyl radical source. The rate of peroxidation in the system was measured by kinetic spectrophotometry (O. D. 504 nm) as the colorless alkali-activated DCFH-DA is oxidized to the chromogen dichlorofluorescein (DCF). Results: Values are means ± SD for samples obtained from the aqueous phase, since DCF is not soluble in PFOB. Conclusions: PFOB does not act as a peroxyl radical scavenger, as the rate of oxidation of DCFH-DA to DCF is the same whether PFOB is present or absent. in the system. Thus, other mechanisms must be responsible for the decreased oxidative damage observed in vitro and in vivo.
|Original language||English (US)|
|Journal||Critical Care Medicine|
|Issue number||1 SUPPL.|
|State||Published - 1999|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine