Abstract

Oxidative stress has been postulated as a mechanism of organ dysfunction - and thus a potential therapeutic target - in sepsis. Lorente and colleagues report increased serum levels of malondialdehyde, a biomarker of oxidative stress-induced lipid peroxidation, in adults with severe sepsis, particularly in non-survivors. While survivors exhibited a decrease in serum malondialdehyde over time, the elevation was sustained in non-survivors. These findings suggest that there is increased oxidative stress in sepsis and that membrane lipids in particular are targeted by free radical species. Further study is required to validate the utility of malondialdehyde as a prognostic biomarker in sepsis and to determine a role for antioxidant therapy.

Highlights

  • Oxidative stress has been postulated as a mechanism of organ dysfunction - and a potential therapeutic target - in sepsis

  • * Correspondence: WeissS@email.chop.edu 1Division of Critical Care Medicine, Department of Anesthesia and Critical Care, The Children’s Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA Full list of author information is available at the end of the article pathogen- or organ-specific reaction

  • Lipid peroxidation results when fatty acids come into contact with reactive oxygen species (ROS), producing a series of reactive aldehydes, including MDA

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Summary

Introduction

Oxidative stress has been postulated as a mechanism of organ dysfunction - and a potential therapeutic target - in sepsis. In a previous issue of Critical Care, Lorente and colleagues demonstrated increased levels of malondialdehyde (MDA), a marker of lipid peroxidation, in the serum of adults with severe sepsis [1]. * Correspondence: WeissS@email.chop.edu 1Division of Critical Care Medicine, Department of Anesthesia and Critical Care, The Children’s Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA Full list of author information is available at the end of the article pathogen- or organ-specific reaction.

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