Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress
This review addresses recent and not so recent works that emphasize on the mechanisms by which liver damage can induce encephalopathy. Hepatic encephalopathy constitutes an intriguing complication in severe liver acute and chronic disease, whose pathophysiology is still not completely understood. In...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2009-04-01
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| Series: | Annals of Hepatology |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1665268119317855 |
| _version_ | 1819103097341870080 |
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| author | Abraham Lemberg Maria Alejandra Fernández |
| author_facet | Abraham Lemberg Maria Alejandra Fernández |
| author_sort | Abraham Lemberg |
| collection | DOAJ |
| description | This review addresses recent and not so recent works that emphasize on the mechanisms by which liver damage can induce encephalopathy. Hepatic encephalopathy constitutes an intriguing complication in severe liver acute and chronic disease, whose pathophysiology is still not completely understood. In this pathology, alterations in normal brain function are associated with morphological and functional impairments of astrocytes and neurons. A wide spectrum of psychoneurological symptoms has been described and the anatomical substratum is usually associated with brain edema and intracranial hypertension, as well as with changes in the function of brain cells. An increase in blood ammonia, toxic to the brain, depends on the activity of the enzyme glutamine synthetase, the glutamine/glutamate cycle and the brain capacity to eliminate toxic substances. When the concentration of the excitotoxic neurotransmitter glutamate is increased, it acts as a toxic agent, especially when its specific transporters are altered and its uptake is decreased. Glutamine has also been recently considered a toxic substance when its concentration is high, and consequently contributes to brain edema. Finally, the formation of reactive oxygen species, basically produced by mitochondria, influence with their toxic action on membrane lipids, proteins and DNA. In conclusion we suggest that at least these four elements are involved directly in the mechanism of hepatic encephalopathy. |
| first_indexed | 2024-12-22T01:45:02Z |
| format | Article |
| id | doaj.art-6ca7e06daa024450b0edc29cd7d15367 |
| institution | Directory Open Access Journal |
| issn | 1665-2681 |
| language | English |
| last_indexed | 2024-12-22T01:45:02Z |
| publishDate | 2009-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Annals of Hepatology |
| spelling | doaj.art-6ca7e06daa024450b0edc29cd7d153672022-12-21T18:43:05ZengElsevierAnnals of Hepatology1665-26812009-04-018295102Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stressAbraham Lemberg0Maria Alejandra Fernández1Department of Pathophysiology. School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina; Address for correspondence:Department of Pathophysiology. School of Pharmacy and Biochemistry, University of Buenos Aires, ArgentinaThis review addresses recent and not so recent works that emphasize on the mechanisms by which liver damage can induce encephalopathy. Hepatic encephalopathy constitutes an intriguing complication in severe liver acute and chronic disease, whose pathophysiology is still not completely understood. In this pathology, alterations in normal brain function are associated with morphological and functional impairments of astrocytes and neurons. A wide spectrum of psychoneurological symptoms has been described and the anatomical substratum is usually associated with brain edema and intracranial hypertension, as well as with changes in the function of brain cells. An increase in blood ammonia, toxic to the brain, depends on the activity of the enzyme glutamine synthetase, the glutamine/glutamate cycle and the brain capacity to eliminate toxic substances. When the concentration of the excitotoxic neurotransmitter glutamate is increased, it acts as a toxic agent, especially when its specific transporters are altered and its uptake is decreased. Glutamine has also been recently considered a toxic substance when its concentration is high, and consequently contributes to brain edema. Finally, the formation of reactive oxygen species, basically produced by mitochondria, influence with their toxic action on membrane lipids, proteins and DNA. In conclusion we suggest that at least these four elements are involved directly in the mechanism of hepatic encephalopathy.http://www.sciencedirect.com/science/article/pii/S1665268119317855Liverbrainmitochondriahyperam-monemiaglutamine/glutamate cycleexcitotoxic neurotransmitter |
| spellingShingle | Abraham Lemberg Maria Alejandra Fernández Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress Annals of Hepatology Liver brain mitochondria hyperam-monemia glutamine/glutamate cycle excitotoxic neurotransmitter |
| title | Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress |
| title_full | Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress |
| title_fullStr | Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress |
| title_full_unstemmed | Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress |
| title_short | Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress |
| title_sort | hepatic encephalopathy ammonia glutamate glutamine and oxidative stress |
| topic | Liver brain mitochondria hyperam-monemia glutamine/glutamate cycle excitotoxic neurotransmitter |
| url | http://www.sciencedirect.com/science/article/pii/S1665268119317855 |
| work_keys_str_mv | AT abrahamlemberg hepaticencephalopathyammoniaglutamateglutamineandoxidativestress AT mariaalejandrafernandez hepaticencephalopathyammoniaglutamateglutamineandoxidativestress |