Hypoxic-ischemic injury in the developing brain: the role of reactive oxygen species originating in mitochondria. Academic Article uri icon

Overview

abstract

  • Mitochondrial dysfunction is the most fundamental mechanism of cell damage in cerebral hypoxia-ischemia and reperfusion. Mitochondrial respiratory chain (MRC) is increasingly recognized as a source for reactive oxygen species (ROS) in the postischemic tissue. Potentially, ROS originating in MRC can contribute to the reperfusion-driven oxidative stress, promoting mitochondrial membrane permeabilization. The loss of mitochondrial membranes integrity during reperfusion is considered as the major mechanism of secondary energy failure. This paper focuses on current data that support a pathogenic role of ROS originating from mitochondrial respiratory chain in the promotion of secondary energy failure and proposes potential therapeutic strategy against reperfusion-driven oxidative stress following hypoxia-ischemia-reperfusion injury of the developing brain.

publication date

  • 2012

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3323863

Digital Object Identifier (DOI)

  • 10.1155/2012/542976

PubMed ID

  • 22548167

Additional Document Info

start page

  • 542976

volume

  • 2012