Ammonia toxicity: from head to toe?
- Dasarathy S Department of Gastroenterology, Hepatology and Pathobiology, Cleveland Clinic, Cleveland, OH, USA.
- Mookerjee RP Liver Failure Group, UCL Institute for Liver and Digestive Health, UCL Medical School, Royal Free Hospital, London, UK.
- Rackayova V Laboratory of Functional and Metabolic Imaging, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
- Rangroo Thrane V Department of Ophthalmology, Haukeland University Hospital, 5021, Bergen, Norway.
- Vairappan B Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Dhanvantri Nagar, Pondicherry, India.
- Ott P Department of Medicine V (Hepatology and Gastroenterology), Aarhus, Denmark.
- Rose CF Hepato-Neuro Laboratory, CRCHUM, Department of Medicine, Université de Montréal, Montréal, Québec, Canada. christopher.rose@umontreal.ca.
- 2016-12-25
Published in:
- Metabolic brain disease. - 2017
Ammonia
Brain
Hepatic encephalopathy
Liver
Muscle
Toxicity
Ammonia
Animals
Brain
Brain Chemistry
Hepatic Encephalopathy
Humans
Hyperammonemia
Muscle, Skeletal
English
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.
- Language
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- English
- Open access status
- green
- Identifiers
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- DOI 10.1007/s11011-016-9938-3
- PMID 28012068
- Persistent URL
- https://sonar.ch/global/documents/212392
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