Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 61, Issue 4, Pages 575-580Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2012.01.012
Keywords
Acute liver failure; Ammonia; Astrocytes; Glutamine; Hepatic encephalopathy; Histidine; Mitochondria; Mitochondrial permeability transition; Oxidative stress
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Funding
- NIH [DK06331]
- Department of Veterans Affairs
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Hepatic encephalopathy (HE) is the major neurological disorder associated with liver disease. It presents in chronic and acute forms, and astrocytes are the major neural cells involved. While the principal etiological factor in the pathogenesis of HE is increased levels of blood and brain ammonia, glutamine, a byproduct of ammonia metabolism, has also been implicated in its pathogenesis. This article reviews the current status of glutamine in the pathogenesis of HE, particularly its involvement in some of the events triggered by ammonia, including mitochondrial dysfunction, generation of oxidative stress, and alterations in signaling mechanisms, including activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-kappa B). Mechanisms by which glutamine contributes to astrocyte swelling/brain edema associated with acute liver failure (ALF) will also be described. Published by Elsevier Ltd.
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