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Metab Brain Dis. 2017 Apr;32(2):529-538. doi: 10.1007/s11011-016-9938-3. Epub 2016 Dec 24.

Ammonia toxicity: from head to toe?

Author information

1
Department of Gastroenterology, Hepatology and Pathobiology, Cleveland Clinic, Cleveland, OH, USA.
2
Liver Failure Group, UCL Institute for Liver and Digestive Health, UCL Medical School, Royal Free Hospital, London, UK.
3
Laboratory of Functional and Metabolic Imaging, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
4
Department of Ophthalmology, Haukeland University Hospital, 5021, Bergen, Norway.
5
Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, Department of Neurosurgery, University of Rochester Medical Center, Rochester, NY, USA.
6
Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Dhanvantri Nagar, Pondicherry, India.
7
Department of Medicine V (Hepatology and Gastroenterology), Aarhus, Denmark.
8
Hepato-Neuro Laboratory, CRCHUM, Department of Medicine, Université de Montréal, Montréal, Québec, Canada. christopher.rose@umontreal.ca.

Abstract

Ammonia is diffused and transported across all plasma membranes. This entails that hyperammonemia leads to an increase in ammonia in all organs and tissues. It is known that the toxic ramifications of ammonia primarily touch the brain and cause neurological impairment. However, the deleterious effects of ammonia are not specific to the brain, as the direct effect of increased ammonia (change in pH, membrane potential, metabolism) can occur in any type of cell. Therefore, in the setting of chronic liver disease where multi-organ dysfunction is common, the role of ammonia, only as neurotoxin, is challenged. This review provides insights and evidence that increased ammonia can disturb many organ and cell types and hence lead to dysfunction.

KEYWORDS:

Ammonia; Brain; Hepatic encephalopathy; Liver; Muscle; Toxicity

PMID:
28012068
DOI:
10.1007/s11011-016-9938-3
[Indexed for MEDLINE]

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