Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis.

Lien, Yeong‐Hau H.; Shapiro, Joseph I.; Chan, Laurence

doi:10.1172/jci115292

Cited by 253 publications

(141 citation statements)

References 32 publications

(60 reference statements)

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“…The latter is a common clinical condition resulting from volume dysregulation and affects between 2.5-5.0% of hospitalized patients and disproportionately affects the young and the elderly (41,42). Depending on the magnitude, hyponatremia can elicit symptoms ranging from emesis and headaches to respiratory arrest, coma, and brain damage (33).…”

Section: Discussionmentioning

confidence: 99%

Taurine Biosynthesis by Neurons and Astrocytes

Vitvitsky

Garg

Banerjee

2011

Journal of Biological Chemistry

102

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The physiological roles of taurine, a product of cysteine degradation and one of the most abundant amino acids in the body, remain elusive. Taurine deficiency leads to heart dysfunction, brain development abnormalities, retinal degradation, and other pathologies. The taurine synthetic pathway is proposed to be incomplete in astrocytes and neurons, and metabolic cooperation between these cell types is reportedly needed to complete the pathway. In this study, we analyzed taurine synthesis capability as reported by incorporation of radioactivity from [ 35 S]cysteine into taurine, in primary murine astrocytes and neurons, and in several transformed cell lines (human (SH-SY5Y) and murine (N1E-115) neuroblastoma, human astrocytoma (U-87MG and 1321 N1), and rat glioma (C6)). Extensive incorporation of radioactivity from [35 S]cysteine into taurine was observed in rat glioma cells as well as in primary mouse astrocytes and neurons, establishing the presence of an intact taurine synthesis pathway in these cells. Interestingly, exposure of cells to cysteine or cysteamine resulted in elevated intracellular hypotaurine without a corresponding increase in taurine levels, suggesting that oxidation of hypotaurine limits taurine synthesis in cells. Consistent with its role as an organic osmolyte, taurine synthesis was stimulated under hypertonic conditions in neurons.Taurine, or ethanesulfonic acid, is one of the most abundant amino acids in the body whose physiological role remains elusive. Its biosynthesis involves the sequential oxidation of cysteine to cysteinesulfinic acid, catalyzed by cysteine dioxygenase, decarboxylation by cysteinesulfinate decarboxylase, and oxidation of the resulting hypotaurine to taurine by a putative hypotaurine dehydrogenase (Fig. 1). The latter enzyme has, however, not been purified to homogeneity and remains uncharacterized (1-3). In fact, it has been suggested that oxidation of hypotaurine to taurine might occur via a nonenzymatic reaction in cells (4 -6). Hypotaurine can also be produced via oxidation of cysteamine, the end product of coenzyme A degradation (Fig. 1). Cysteamine oxidation is catalyzed by 2-aminoethanethiol dioxygenase, which is widely expressed in mammalian tissues (7).Although it is generally believed that taurine cannot be further metabolized and is excreted by the kidney or as a bile component, there are several older reports in the literature on the conversion of taurine to isethionic acid in mammalian tissues (8 -11). Various roles have been ascribed to taurine, including regulation of osmotic pressure (12-14), neuromodulatory (3, 15) and immunomodulatory (16) factors, and as an antioxidant for detoxifying hypochlorous acid, forming taurine chloramine (12). Taurine deficiency is associated with heart dysfunction, brain development abnormalities, retinal degradation, and other pathologies (3, 17). Taurine is actively transported into cells by a specific Na ϩ -dependent transporter (TAUT) and accumulates to high concentrations particularly in the liver, muscle, and retina. ...

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Section: Discussionmentioning

confidence: 99%

Taurine Biosynthesis by Neurons and Astrocytes

Vitvitsky

Garg

Banerjee

2011

Journal of Biological Chemistry

102

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“…Brunner et al (7) found that the initial severity and duration of the hyponatremia were crucial factors in the development ofpontine lesions. In an animal study, Lien et al (8) reported that a rapid correction of hyponatremia due to Na infusion provokes an overshoot of intracellular Na and Cl levels in brain tissues with decreased ideogenic osmol. MRIhas been shown to be effective to detect disorders such as CPM.…”

Section: Discussionmentioning

confidence: 99%

Cortical Laminar Necrosis and Central Pontine Myelinolysis in a Patient with Sheehan Syndrome and Severe Hyponatremia.

et al. 1996

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Hypoxic encephalopathy and osmotic demyelination are independent clinical entities. We describe a rare case with these two complications as demonstratedby magnetic resonance imaging (MRI). A 58-year-old womanhad adrenal crises twice a decade due to Sheehan syndrome. At the second crisis, hyponatremia wasremarkable with consciousness disturbance which was rapidly corrected by intraveneous administration of glucocorticoid and hypertonic saline. The maneuver improved consciousness disturbance, but resulted in hypokalemic ventricular fibrillation with circulatory failure. After the normalization of the circulation, however, her consciousness level deteriorated again. Repeated brain MRIrevealed acute and chronic phases of cortical laminar necrosis and central pontine myelinolysis.

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“…По результатам нашей работы, у мышей опыта через 60 дней после введения СТЗ наблюдается достоверное повышение уровня таурина. Считается, что таурин вместе с креатином и мио-инозитолом участвует в осмотической регуляции мозга (Lien et al, 1990(Lien et al, , 1991. Увеличение уровня таурина отмечается также в головном мозге крыс с СТЗ-индуцированным сахарным диабетом (Rose et al, 2000).…”

Section: физиологическая генетикаunclassified

The effect of a single administration of streptozotocin on hippocampus metabolites in NODSCID mice

Tur¹,

Shevelev²,

Sharapova³

et al. 2018

Vestn. VOGiS

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The significant increase in the number of people diag nosed with diabetes mellitus in recent years makes studies of this problem topical. The persistent hyper glycemia accompanying the development and course of type 1 diabetes mellitus (T1DM) can affect the func tional and structural levels of the organization of the central nervous system. These changes may be medi ated by metabolic aberrations. Magnetic resonance spectroscopy (MRS) is a common method of intravital detection of metabolic reactions. In this study, MRS of the hippocampus of NOD.CB17 Prkdc scid /NcrCrl mice (NODSCID) was performed 4 days after the admini stration of streptozotocin (STZ) to assess the effect of STZ itself, and 60 days after the administration of STZ to another group of animals to assess the effect of chronic hyperglycemia caused by the delayed ef fect of STZ, involving the death of pancreatic βcells. The simulation of T1DM by STZ administration is used worldwide. Nevertheless, the question remains whether there is a shortterm effect of the introduc tion of STZ at the level of hippocampal metabolites recorded by MRS. The comparison of experimental and control animal groups revealed no effect of STZ on metabolites in the hippocampus of NODSCID mice on day 4 after its administration. In contrast, another comparison of the experimental and control animals on day 60 after STZ administration showed elevated contents of alanine and taurine, and a reduced lactate content. Thus, the introduction of STZ itself does not affect the metabolism of the hippocampus, and MRS is a promising method for assessing the effect of T1DM on brain metabolism in animals.Key words: type 1 diabetes mellitus; NOD.CB17 Prkdc scid /NcrCrl mice; magnetic resonance spectro scopy; streptozotocin; hippocampus.Значимое увеличение за последние годы числа людей с установ ленным диагнозом «сахарный диабет» выводит исследования, посвященные этой проблеме, в число наиболее актуальных. Про должительная гипергликемия, сопровождающая развитие и тече ние сахарного диабета 1го типа (СД1), может отразиться на функ циональном и структурном уровне организации работы головного мозга. В основе подобных реакций может лежать изменение мета болизма. Общепринятым методом прижизненного выявления ме та болических реакций в организме служит магнитнорезонансная спектроскопия (МРС). В настоящей работе для оценки влияния стрептозотоцина (СТЗ) и хронической гипергликемии, обуслов ленной отсроченным эффектом СТЗ, реализованным через гибель βклеток поджелудочной железы, проведена МРС гиппокампа мы шей линии NOD.CB17Prkdc scid /NcrCrl (NODSCID) через 4 и 60 дней после введения СТЗ. Модель СД1 с введением СТЗ -самая распро страненная в мировой практике. Вместе с тем остается открытым вопрос -существует ли краткосрочный эффект введения СТЗ на уровень детектируемых с помощью МРС метаболитов гиппокампа животных. В результате сравнения опытной группы животных с контролем выявлено отсутствие влияния СТЗ на метаболиты гип покампа мышей NODSCID на 4й день после его введения. Однако в другом сравнении живо...

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Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis.

Cited by 253 publications

References 32 publications

Taurine Biosynthesis by Neurons and Astrocytes

Taurine Biosynthesis by Neurons and Astrocytes

Cortical Laminar Necrosis and Central Pontine Myelinolysis in a Patient with Sheehan Syndrome and Severe Hyponatremia.

The effect of a single administration of streptozotocin on hippocampus metabolites in NODSCID mice

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