Abstract
Introduction: Oxidative stress is one of the basic mechanisms of tissue injury, having been implicated in various processes such as aging, cancer, sepsis, inflammation, as well as cardiovascular and respiratory diseases. In view of the fact that PFOB attenuates oxidative lung injury in vivo, we hypothesized that this finding might be due, in part, to a direct protective effect of PFOB against reactive oxygen species-associated injury Methods: We tested the hypothesis by studying an in vitro non-biological system. Linoleic acid (3mM) was emulsified into an aqueous buffer (PBS) by a detergent (SDS, 250μM). Linoleic acid/SDS micelles were formed by agitation and sonication of the emulsion. Oxidative stress was applied by adding various concentrations (2-50mM) of AAPH, a peroxyl radical generator, to the emulsion in the absence (control) or presence (PFOB) of PFOB at 37°C. Malondialdehyde (MDA) was used as an indicator of oxidation of linoleic acid micelles. MDA concentrations were measured in samples originated from the emulsion over a period of 4 hours. Results: Values are means ± SD for the 20mM AAPH experiment. Experiments with other concentrations of AAPH resulted in similar patterns. *p < 0.05 vs baseline. † p < 0.05 vs PFOB. Conclusions: PFOB attenuates oxidative damage to synthetic linoleic acid micelles from various concentrations of AAPH in a non-biological system. This effect may account for the decreased oxidative damage to injury-prone tissues exposed to PFOB.
| Original language | English (US) |
|---|---|
| Journal | Critical Care Medicine |
| Volume | 27 |
| Issue number | 1 SUPPL. |
| State | Published - 1999 |
| Externally published | Yes |
Fingerprint
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
Cite this
Perflubron (PFOB) protects against fatty acid oxidation in a non-biological, in vitro model. / Rotta, Alexandre T.; Gunnarsson, Björn; Hernan, Lynn J.; Steinhorn, David M.
In: Critical Care Medicine, Vol. 27, No. 1 SUPPL., 1999.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Perflubron (PFOB) protects against fatty acid oxidation in a non-biological, in vitro model
AU - Rotta, Alexandre T.
AU - Gunnarsson, Björn
AU - Hernan, Lynn J.
AU - Steinhorn, David M.
PY - 1999
Y1 - 1999
N2 - Introduction: Oxidative stress is one of the basic mechanisms of tissue injury, having been implicated in various processes such as aging, cancer, sepsis, inflammation, as well as cardiovascular and respiratory diseases. In view of the fact that PFOB attenuates oxidative lung injury in vivo, we hypothesized that this finding might be due, in part, to a direct protective effect of PFOB against reactive oxygen species-associated injury Methods: We tested the hypothesis by studying an in vitro non-biological system. Linoleic acid (3mM) was emulsified into an aqueous buffer (PBS) by a detergent (SDS, 250μM). Linoleic acid/SDS micelles were formed by agitation and sonication of the emulsion. Oxidative stress was applied by adding various concentrations (2-50mM) of AAPH, a peroxyl radical generator, to the emulsion in the absence (control) or presence (PFOB) of PFOB at 37°C. Malondialdehyde (MDA) was used as an indicator of oxidation of linoleic acid micelles. MDA concentrations were measured in samples originated from the emulsion over a period of 4 hours. Results: Values are means ± SD for the 20mM AAPH experiment. Experiments with other concentrations of AAPH resulted in similar patterns. *p < 0.05 vs baseline. † p < 0.05 vs PFOB. Conclusions: PFOB attenuates oxidative damage to synthetic linoleic acid micelles from various concentrations of AAPH in a non-biological system. This effect may account for the decreased oxidative damage to injury-prone tissues exposed to PFOB.
AB - Introduction: Oxidative stress is one of the basic mechanisms of tissue injury, having been implicated in various processes such as aging, cancer, sepsis, inflammation, as well as cardiovascular and respiratory diseases. In view of the fact that PFOB attenuates oxidative lung injury in vivo, we hypothesized that this finding might be due, in part, to a direct protective effect of PFOB against reactive oxygen species-associated injury Methods: We tested the hypothesis by studying an in vitro non-biological system. Linoleic acid (3mM) was emulsified into an aqueous buffer (PBS) by a detergent (SDS, 250μM). Linoleic acid/SDS micelles were formed by agitation and sonication of the emulsion. Oxidative stress was applied by adding various concentrations (2-50mM) of AAPH, a peroxyl radical generator, to the emulsion in the absence (control) or presence (PFOB) of PFOB at 37°C. Malondialdehyde (MDA) was used as an indicator of oxidation of linoleic acid micelles. MDA concentrations were measured in samples originated from the emulsion over a period of 4 hours. Results: Values are means ± SD for the 20mM AAPH experiment. Experiments with other concentrations of AAPH resulted in similar patterns. *p < 0.05 vs baseline. † p < 0.05 vs PFOB. Conclusions: PFOB attenuates oxidative damage to synthetic linoleic acid micelles from various concentrations of AAPH in a non-biological system. This effect may account for the decreased oxidative damage to injury-prone tissues exposed to PFOB.
UR - http://www.scopus.com/inward/record.url?scp=25044474969&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=25044474969&partnerID=8YFLogxK
M3 - Article
VL - 27
JO - Critical Care Medicine
JF - Critical Care Medicine
SN - 0090-3493
IS - 1 SUPPL.
ER -