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  • Poster presentation
  • Open Access

N-Acetylcysteine inhibits peroxynitrite-mediated damage in oleic acid-induced lung injury

  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Critical Care20048 (Suppl 1) :P204

https://doi.org/10.1186/cc2671

  • Published:

Keywords

  • Oleic Acid
  • Lung Injury
  • Acute Lung Injury
  • Lung Injury Model
  • Lung Histopathology

Since oleic acid (OA) induces morphologic and cellular changes similar to those observed in human acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), it has become a widely used model to investigate the effects of several agents on pathogenesis of lung injury. The antioxidant, anti-inflammatory and antiapoptotic properties of N-acetylcysteine (NAC) have been documented in many lung injury models [1]. In this study, we evaluated the role of NAC in an OA-induced lung injury model by measuring myeloperoxidase (MPO) activity, malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels in lung tissue.

Five groups (sham, NAC, OA, pre-OA-NAC and post-OA-NAC) were determined. ALI/ARDS was induced by intravenous (IV) administration of OA. The pre-OA-NAC group received IV NAC 15 min before OA infusion and the post-OA-NAC group received IV NAC 2 hours after OA infusion. In both of the NAC treatment groups, blood and tissue samples were collected 4 hours after OA infusion, independent of the time of NAC infusion.

The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in the OA group, and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (P = 0.0001). Lung histopathology was also protected by NAC in this OA-induced experimental lung injury model.

In conclusion, the present study demonstrates that oleic acid induces myeloperoxydase activation and consequently increases 3-NT and MDA levels in lung tissue. Our data suggest that elevated 3-NT levels in lung tissue represent the role of excessive formation of peroxynitrite and the efficacy of NAC treatment in the prevention of peroxynitrite-mediated OA-induced lung injury. Due to its antioxidant and anti-inflammatory properties, NAC seems to be a promising agent in treatment of critically ill patients with lung injury states.

Authors’ Affiliations

(1)
Mersin University, Turkey

References

  1. Ozdulger A, Cinel I, Koksel O, et al.: The protective effect of N -acetylecysteine on apoptotic lung injury in CLP-induced sepsis model. Shock 2003, 19: 366-372. 10.1097/00024382-200304000-00012View ArticlePubMedGoogle Scholar

Copyright

© BioMed Central Ltd. 2004

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