Abstract:
:Lactic acid accumulation has been implicated in the evolution of brain damage after ischemia. Since compartmentation of lactate may play a role in acid-base balance, lactate release from gerbil hippocampal slices was examined during a number of metabolic stresses including elevated [K+]e, ischemia, anoxia, and aglycemia. Slices were preincubated for 1 hr in artificial cerebrospinal fluid (ACSF) equilibrated with 95% O2/5% CO2 (pH 7.4 at 37 degrees C) and then transferred to tubes containing 300 microliters of test medium. The rate of lactate release in control slices was 9.64 nmol/min/mg protein and increased 2.6- and 3.2-fold in the presence of 60 mM potassium and anoxia, whereas the rate of lactate release was decreased by 50 and 25% during ischemia and aglycemia. Lactate release was temperature dependent and was only minimally influenced by removing Ca2+ or by adding 5 mM d-lactate to the ACSF. In contrast, pyruvate inhibited lactate release with an apparent Ki of 2.4 mM. The results suggest that lactate can be released from cells via a saturable and stereospecific lactate transporter with an apparent Km of 10.7 mM and Vmax of 43.7 nmol/mg protein/min. Such a relatively high-capacity transporter system can rapidly equilibrate brain lactate but is probably not involved in regulating intracellular acid-base balance.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Assaf HM,Ricci AJ,Whittingham TS,LaManna JC,Ratcheson RA,Lust WDdoi
10.1007/BF00999841subject
Has Abstractpub_date
1990-09-01 00:00:00pages
143-54issue
3eissn
0885-7490issn
1573-7365journal_volume
5pub_type
杂志文章abstract::The availability of an animal model is crucial in studying the pathophysiological mechanisms of disease and to test possible therapies. Now, there are several models for the study of liver diseases, but there still remains a lack of a satisfactory animal model of chronic liver disease with hepatic encephalopathy (HE) ...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-005-7925-1
更新日期:2005-12-01 00:00:00
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abstract::Hepatic encephalopathy (HE) represents a nervous system disorder caused due to liver dysfunction. HE is broadly classified as acute/overt and moderate-minimal HE. Since HE syndrome severely affects quality of life of the patients and it may be life threatening, it is important to develop effective therapeutic strategy...
journal_title:Metabolic brain disease
pub_type: 杂志文章
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-006-9002-9
更新日期:2006-03-01 00:00:00
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journal_title:Metabolic brain disease
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doi:10.1007/s11011-014-9615-3
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journal_title:Metabolic brain disease
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abstract::Glutaric aciduria type 1 is a neurometabolic disorder, caused by riboflavin-dependent glutaryl-CoA dehydrogenase deficiency. As its consequence, accumulation of the putatively neurotoxic metabolites (glutaric and 3-hydroxyglutaric acids) in body tissues, but especially within the brain, is observed. Estimated incidenc...
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-010-9195-9
更新日期:2010-06-01 00:00:00
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF01000159
更新日期:1992-09-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9581-9
更新日期:2015-02-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-018-0239-x
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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更新日期:2015-10-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-014-9504-9
更新日期:2014-09-01 00:00:00
abstract::Adult-onset type II citrullinemia (CTLN2), characterized by a liver-specific deficiency of urea cycle enzyme, argininosuccinate synthetase, is caused by mutations in SLC25A13 that encodes a calcium binding mitochondrial solute carrier protein, citrin. Citrin deficiency causes not only CTLN2 but also neonatal intrahepa...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1023/a:1021961919148
更新日期:2002-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:
更新日期:1997-09-01 00:00:00
abstract::Although gaseous ammonia (NH3) can freely enter cells through the plasma membrane where NH3 is cyto(neuro)toxic, NH3 and ionic ammonia (NH4+) contents have not been studied in biological materials. We developed a new method for measurement of expiratory NH3 concentration, which may reflect blood NH3 concentrations. Th...
journal_title:Metabolic brain disease
pub_type: 临床试验,杂志文章
doi:
更新日期:1997-06-01 00:00:00
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journal_title:Metabolic brain disease
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doi:10.1007/s11011-016-9879-x
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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更新日期:2016-10-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-020-00552-z
更新日期:2020-06-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9550-3
更新日期:2015-04-01 00:00:00
abstract::A rat model of glucose-precipitated Wernicke's encephalopathy (WE) has been developed in which glucose loading (10 g/kg, i.p.) of ataxic thiamin-deficient (TD) rats induced episodes of gross neurological dysfunction and sometimes death. The acute effects of a glucose load on the neurological state of thiamin-replete c...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020653312697
更新日期:1999-03-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/BF01001350
更新日期:1988-03-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF00999694
更新日期:1987-12-01 00:00:00