Mechanisms of ammonia-induced astrocyte swelling

Michael D Norenberg, K. V. Rama Rao, A. R. Jayakumar

Research output: Contribution to journalArticle

126 Citations (Scopus)

Abstract

Astrocyte swelling represents the major factor responsible for the brain edema associated with fulminant hepatic failure (FHF). The edema may be of such magnitude as to increase intracranial pressure leading to brain herniation and death. Of the various agents implicated in the generation of astrocyte swelling, ammonia has had the greatest amount of experimental support. This article reviews mechanisms of ammonia neurotoxicity that contribute to astrocyte swelling. These include oxidative stress and the mitochondrial permeability transition (MPT). The involvement of glutamine in the production of cell swelling will be highlighted. Evidence will be provided that glutamine induces oxidative stress as well as the MPT, and that these events are critical in the development of astrocyte swelling in hyperammonemia.

Original languageEnglish
Pages (from-to)303-318
Number of pages16
JournalMetabolic Brain Disease
Volume20
Issue number4
DOIs
StatePublished - Dec 1 2005

Fingerprint

Ammonia
Astrocytes
Swelling
Glutamine
Oxidative stress
Permeability
Oxidative Stress
Brain
Hyperammonemia
Brain Death
Intracranial Hypertension
Acute Liver Failure
Brain Edema
Edema

Keywords

  • Ammonia
  • Aquaporin-4
  • Cell swelling
  • Glutamine
  • Glutathione
  • Lactate
  • Mitochondrial permeability transition
  • Neurosteroids
  • Oxidative stress
  • Peripheral benzodiazepine receptor

ASJC Scopus subject areas

  • Clinical Neurology
  • Biochemistry
  • Neuroscience(all)

Cite this

Mechanisms of ammonia-induced astrocyte swelling. / Norenberg, Michael D; Rama Rao, K. V.; Jayakumar, A. R.

In: Metabolic Brain Disease, Vol. 20, No. 4, 01.12.2005, p. 303-318.

Research output: Contribution to journalArticle

Norenberg, Michael D ; Rama Rao, K. V. ; Jayakumar, A. R. / Mechanisms of ammonia-induced astrocyte swelling. In: Metabolic Brain Disease. 2005 ; Vol. 20, No. 4. pp. 303-318.
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