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Titolo:
Role of glutamine in cerebral nitrogen metabolism and ammonia neurotoxicity
Autore:
Cooper, AJL;
Indirizzi:
Cornell Univ, Weill Med Coll, Burke Med Res Inst, White Plains, NY 10605 USA Cornell Univ White Plains NY USA 10605 s Inst, White Plains, NY 10605 USA Cornell Univ, Weill Med Coll, Dept Biochem & Neurol, New York, NY USA Cornell Univ New York NY USA ll, Dept Biochem & Neurol, New York, NY USA Cornell Univ, Weill Med Coll, Dept Neurosci, New York, NY USA Cornell Univ New York NY USA l Med Coll, Dept Neurosci, New York, NY USA
Titolo Testata:
MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS
fascicolo: 4, volume: 7, anno: 2001,
pagine: 280 - 286
SICI:
1080-4013(2001)7:4<280:ROGICN>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-BRAIN-BARRIER; ACETYL-L-CARNITINE; CHAIN AMINO-ACIDS; RAT-BRAIN; ACUTE HYPERAMMONEMIA; CULTURED ASTROCYTES; NITRIC-OXIDE; ASPARTATE-AMINOTRANSFERASE; METHIONINE SULFOXIMINE; HEPATIC-ENCEPHALOPATHY;
Keywords:
ammonia; cerebral nitrogen metabolism; glutamate; glutamine; hyperammonemia;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
79
Recensione:
Indirizzi per estratti:
Indirizzo: Cooper, AJL Cornell Univ, Weill Med Coll, Burke Med Res Inst, 785 Mamaroneck Ave, White Plains, NY 10605 USA Cornell Univ 785 Mamaroneck Ave White Plains NY USA 10605 USA
Citazione:
A.J.L. Cooper, "Role of glutamine in cerebral nitrogen metabolism and ammonia neurotoxicity", MENT RET D, 7(4), 2001, pp. 280-286

Abstract

Ammonia enters the brain by diffusion from the blood or cerebrospinal fluid, or is formed in situ from the metabolism of endogenous nitrogen-containing substances. Despite its central importance in nitrogen homeostasis, excess ammonia is toxic to the central nervous system and its concentration in the brain must be kept low. This is accomplished by the high activity of glutamine synthetase, which is localized in astrocytes and which permits efficient detoxification of incoming or endogenously generated ammonia. The location also permits the operation of an intercellular glutamine cycle. In this cycle, glutamate released from nerve terminals is taken up by astrocyteswhere it is converted to glutamine. Glutamine is released to the extracellular fluid to be taken up into the nerve cells, where it is converted back to glutamate by the action of glutaminase. Most extrahepatic organs lack a complete urea cycle, and for many organs, including the brain, glutamine represents a temporary storage form of waste nitrogen. As such, glutamine waslong thought to be harmless to the brain. However, recent evidence suggests that excess glutamine is neurotoxic. Hyperammonemic syndromes (e.g., liver disease, inborn errors of the urea cycle, Reye's disease) consistently cause astrocyte pathology. Evidence has been presented that hyperammonemia results in increased formation of glutamine directly in astrocytes, thereby generating an osmotic stress to these cells. This osmotic stress results in impaired astrocyte function, which in turn leads to neuronal dysfunction. In this review a brief overview is presented of the role of glutamine in normal brain metabolism and in the pathogenesis of hyperammonemic syndromes. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/07/20 alle ore 04:39:04