Neurochemical Research

, Volume 35, Issue 1, pp 1–12

Oxidative Mechanisms of Brain Dysfunction During Sepsis

  • Felipe Dal-Pizzol
  • Cristiane Ritter
  • Omar J. Cassol-Jr
  • Gislaine T. Rezin
  • Fabrícia Petronilho
  • Alexandra I. Zugno
  • João Quevedo
  • Emilio L. Streck
Overview

DOI: 10.1007/s11064-009-0043-4

Cite this article as:
Dal-Pizzol, F., Ritter, C., Cassol-Jr, O.J. et al. Neurochem Res (2010) 35: 1. doi:10.1007/s11064-009-0043-4

Abstract

Oxidative stress has drawn a lot of attention in the past few decades, since it has been reported to participate in the mechanism of many diseases. Therefore, it seemed to be a good rationale to aim oxidative stress on therapeutic research. Sepsis is a complex systemic syndrome characterized by an imbalance between pro- and anti-inflammatory responses to a pathogen; its pathophysiology is a dynamic process which involves components of the immune system, the coagulation pathway, parenchymal cells, and the endocrine and metabolic pathways. It is well characterized that oxidative stress plays a crucial role in sepsis development, but the relation between central nervous system dysfunction and oxidative stress during sepsis is not well understood. Thus, we here summarize the current knowledge on the role of free radicals in the development of brain dysfunction in sepsis focusing on oxidative damage and the redox control of brain inflammatory pathways.

Keywords

SepsisOxidative stressCentral nervous systemBrain injuryRedox signaling

Abbreviations

AP-1

Activator protein-1

ARE

Antioxidant response element

ATP

Adenosine triphosphate

BBB

Blood-brain-barrier

CAT

Catalase

CLP

Cecal ligation and perforation

CNS

Central nervous system

DNA

Deoxyribonucleic acid

ERK

Extracellular signal-regulated kinase

ETC

Electron transport chain

H2O2

Hydrogen peroxide

IKK

NF-κB (IκB)-kinase

IL-1

Interleukin-1

IL-1RA

Interleukin-1 receptor antagonist

IL-1β

Interleukin-1β

IL-2

Interleukin-2

IL-6

Interleukin-6

iNOS

Inducible nitric oxide synthase

IRAK1

Interleukin-1 receptor-associated kinase 1

IRAK4

Interleukin-1 receptor-associated kinase 4

JNK

Jun N-terminal kinase

LPS

Lipopolysaccharide

MAPK

Mitogen-activated protein kinase

MCP-1

Monocyte chemotactic protein-1

MKP-1

MAPK phosphatase-1

MMP

Matrix metalloproteinases

mRNA

Messenger ribonucleic acid

MyD88

Myeloid differentiation primary-response protein 88

NADPH

Nicotinamide adenine dinucleotide phosphate

NF-κB

Nuclear factor kappa-B

NO

Nitric oxide

NOS

Nitric oxide synthase

NrF2

Nuclear factor-E2 related factor 2

OXPHOS

Oxidative phosphorylation

PI3K

Phosphatidylinositol 3-kinase

PKC

Protein kinase C

RNS

Reactive nitrogen species

ROS

Reactive oxygen species

SE

Septic encephalopathy

SOD

Superoxide dismutase

TAK1

Transforming growth factor-β-activated kinase

TLR

Toll-like receptors

TNF-α

Tumor necrosis factor-alpha

TRAF6

Tumor necrosis factor receptor-associated factor 6

XO

Xanthine oxidase

Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  • Felipe Dal-Pizzol
    • 1
    • 2
  • Cristiane Ritter
    • 1
    • 2
  • Omar J. Cassol-Jr
    • 1
    • 2
  • Gislaine T. Rezin
    • 1
    • 2
  • Fabrícia Petronilho
    • 1
    • 2
  • Alexandra I. Zugno
    • 3
    • 2
  • João Quevedo
    • 3
    • 2
  • Emilio L. Streck
    • 1
    • 2
  1. 1.Laboratório de Fisiopatologia Experimental, Programa de Pós-graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da SaúdeUniversidade do Extremo Sul CatarinenseCriciúmaBrazil
  2. 2.Instituto Nacional de Ciência e Tecnologia Translacional em MedicinaUniversidade do Extremo Sul CatarinenseCriciúmaBrazil
  3. 3.Laboratório de Neurociências, Programa de Pós-graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da SaúdeUniversidade do Extremo Sul CatarinenseCriciúmaBrazil