Journal of Bioenergetics and Biomembranes

, Volume 36, Issue 4, pp 369–373

Mitochondrial Impairment in the Developing Brain After Hypoxia–Ischemia

  • Henrik Hagberg
Article

DOI: 10.1023/B:JOBB.0000041770.00567.4f

Cite this article as:
Hagberg, H. J Bioenerg Biomembr (2004) 36: 369. doi:10.1023/B:JOBB.0000041770.00567.4f

Abstract

The pattern of cell death in the immature brain differs from that seen in the adult CNS. During normal development, more than half of the neurons are removed through apoptosis, and mediators like caspase-3 are highly upregulated. The contribution of apoptotic mechanisms in cell death appears also to be substantial in the developing brain, with a marked activation of downstream caspases and signs of DNA fragmentation. Mitochondria are important regulators of cell death through their role in energy metabolism and calcium homeostasis, and their ability to release apoptogenic proteins and to produce reactive oxygen species. We find that secondary brain injury is preceded by impairment of mitochondrial respiration, signs of membrane permeability transition, intramitochondrial accumulation of calcium, changes in the Bcl-2 family proteins, release of proapoptotic proteins (cytochrome C, apoptosis inducing factor) and downstream activation of caspase-9 and caspase-3 after hypoxia-ischemia. These data support the involvement of mitochondria-related mechanisms in perinatal brain injury.

Hypoxia-ischemiamitochondriacaspasesN-methyl-D-aspartatenitric oxideapoptosis-inducing factorcytochrome Cimmaturemembrane permeability transitionBcl-2

Copyright information

© Springer Science+Business Media, Inc. 2004

Authors and Affiliations

  • Henrik Hagberg
    • 1
  1. 1.Perinatal Center, Department for the Health of Women and ChildrenSahlgrenska AcademyEast Hospital, 416 85