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Updated: Jun 10, 2026
Analyzing Oxidative Stress in Murine Intestinal Organoids using Reactive Oxygen Species-Sensitive Fluorogenic Probe
Published on: September 17, 2021
Oxidative stress as a novel target in pediatric sepsis management
Bettina von Dessauer1, Jazmina Bongain, Víctor Molina
1Pediatric Intensive Care Unit, Doctor Roberto del Río Children's Hospital, Santiago, Chile.
Insights
Sepsis causes pediatric intensive care unit deaths, potentially driven by oxidative stress. Targeting antioxidant pathways, like mitochondria, may improve outcomes in critically ill children.
Area of Science:
- Biomedical science
- Pediatric critical care
- Oxidative stress research
Background:
- Sepsis with multisystem organ dysfunction syndrome (MODS) is a leading cause of pediatric intensive care unit mortality.
- Increased reactive oxygen species (ROS) may contribute to inflammatory tissue injury and hypoxia via microvascular dysfunction.
- Impaired mitochondrial oxygen utilization, not just oxygen delivery, is implicated in MODS development.
Purpose of the Study:
- To investigate the role of reactive oxygen species in sepsis-induced MODS.
- To explore potential pharmacologic targets for antioxidant interventions.
- To assess the utility of oxidative stress biomarkers for guiding therapy.
Main Methods:
- Review of existing literature on sepsis pathophysiology and oxidative stress.
- Discussion of potential therapeutic targets including mitochondria and NADPH oxidase.
- Consideration of early recognition and biomarker-guided antioxidant strategies.
Main Results:
- Reactive oxygen species plausibly mediate sepsis pathophysiology.
- Current guidelines lack antioxidant enhancement strategies.
- Specific targets like mitochondria and NADPH oxidase require exploration.
Conclusions:
- Further research is needed to support antioxidant interventions in pediatric sepsis.
- Targeting oxidative damage mechanisms may improve outcomes.
- Biomarker-guided antioxidant therapy could offer a novel strategy for critically ill children.
Abstract:
Sepsis with secondary multisystem organ dysfunction syndrome is the leading cause of death in the pediatric intensive care unit. Increased reactive oxygen species may influence circulating and endothelial cells, contributing to inflammatory tissue injury and explaining the tissue hypoxia paradigm based on microvascular dysfunction. An impaired mitochondrial cellular oxygen utilization, rather than inadequate oxygen delivery, was claimed to play a more important role in the development of multisystem organ dysfunction syndrome. Anyway, it seems plausible that reactive oxygen species can mediate the pathophysiologic processes occurring in sepsis. However, the consensus guidelines for the management of patients with these conditions do not include the enhancement of antioxidant potential. Therefore, further investigation is needed to support interventions aimed to attenuate the severity of the systemic compromise by abrogating the mechanism of oxidative damage. Antioxidant supplementation currently in use lacks a mechanistic support. Specific pharmacologic targets, such as mitochondria or Nicotinamide Adenine Dinucleotide Phosphate-Oxidase (NADPH) oxidase system, need to be explored. Furthermore, the early recognition of oxidative damage in these seriously ill patients and the usefulness of oxidative stress biomarkers to define a cut point for more successful therapeutic antioxidant interventions to be instituted would offer a new strategy to improve the outcome of critically ill children.
