Neuro-oxidative-nitrosative stress in sepsis

Damian Bailey, Ronan MG Berg, Kirsten Møller

Research output: Contribution to journalArticlepeer-review


Neuro-oxidative-nitrosative stress may prove the molecular basis underlying brain dysfunction in sepsis. In the current review, we describe how sepsis-induced reactive oxygen and nitrogen species (ROS/RNS) trigger lipid peroxidation chain reactions throughout the cerebrovasculature and surrounding brain parenchyma, due to failure of the local antioxidant systems. ROS/RNS cause structural membrane damage, induce inflammation, and scavenge nitric oxide (NO) to yield peroxynitrite (ONOO(-)). This activates the inducible NO synthase, which further compounds ONOO(-) formation. ROS/RNS cause mitochondrial dysfunction by inhibiting the mitochondrial electron transport chain and uncoupling oxidative phosphorylation, which ultimately leads to neuronal bioenergetic failure. Furthermore, in certain 'at risk' areas of the brain, free radicals may induce neuronal apoptosis. In the present review, we define a role for ROS/RNS-mediated neuronal bioenergetic failure and apoptosis as a primary mechanism underlying sepsis-associated encephalopathy and, in sepsis survivors, permanent cognitive deficits.

Original languageEnglish
Pages (from-to)1532 - 1544
Number of pages13
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number7
Publication statusPublished - 13 Apr 2011


  • apoptosis
  • cognitive dysfunction
  • inflammation
  • reactive oxygen-nitrogen species
  • sepsis-associated encephalopathy


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