Changes in the activity of γ-glutamyl transpeptidase in brain microvessels, astroglial cells and synaptosomes derived from rats with hepatic encephalopathy

Šťastný, F; Hilgier, Wojciech; Albrecht, Jan; Lisý, V.

doi:10.1016/0304-3940(88)90529-0

Cited by 27 publications

(1 citation statement)

References 23 publications

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“…These effects appeared to be due to ammonia-induced functional impairment of LNAA transport at the BBB. In rats in which HA was executed by urease administration, the impairment was found closely correlated with the rise in brain Gln content (Bachmann and Colombo 1983), while in the cortical capillaries the increased Try-Gln exchange could be related to the raised γ-glutamyl-transpeptidase (GGT) activity (Stastný et al 1988). Because GGT participates in LNAA transport and its activity was found to be increased in brain capillaries from hyperammonemic rats, a hypothesis has been put forward that GGT is involved in triggering the outward transport of the excess of Gln from brain (Gorgievski-Hrisoho et al 1986).…”

Section: Transcellular Passage Of Different Molecules Across the Endomentioning

confidence: 99%

Alterations of Blood Brain Barrier Function in Hyperammonemia: An Overview

Skowrońska

Albrecht

2011

Neurotox Res

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Ammonia is a neurotoxin involved in the pathogenesis of neurological conditions associated with hyperammonemia, including hepatic encephalopathy, a condition associated with acute—(ALF) or chronic liver failure. This article reviews evidence that apart from directly affecting the metabolism and function of the central nervous system cells, ammonia influences the passage of different molecules across the blood brain barrier (BBB). A brief description is provided of the tight junctions, which couple adjacent cerebral capillary endothelial cells to each other to form the barrier. Ammonia modulates the transcellular passage of low-to medium-size molecules, by affecting their carriers located at the BBB. Ammonia induces interrelated aberrations of the transport of the large neutral amino acids and aromatic amino acids (AAA), whose influx is augmented by exchange with glutamine produced in the course of ammonia detoxification, and maybe also modulated by the extracellularly acting gamma-glutamyl moiety transferring enzyme, gamma-glutamyl-transpeptidase. Impaired AAA transport affects neurotransmission by altering intracerebral synthesis of catecholamines (serotonin and dopamine), and producing “false neurotransmitters” (octopamine and phenylethylamine). Ammonia also modulates BBB transport of the cationic amino acids: the nitric oxide precursor, arginine, and ornithine, which is an ammonia trap, and affects the transport of energy metabolites glucose and creatine. Moreover, ammonia acting either directly or in synergy with liver injury-derived inflammatory cytokines also evokes subtle increases of the transcellular passage of molecules of different size (BBB “leakage”), which appears to be responsible for the vasogenic component of cerebral edema associated with ALF.

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Section: Transcellular Passage Of Different Molecules Across the Endomentioning

confidence: 99%

Alterations of Blood Brain Barrier Function in Hyperammonemia: An Overview

Skowrońska

Albrecht

2011

Neurotox Res

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Utilization of cysteine and cysteine precursors for the synthesis of glutathione in astroglial cultures: Preference for cystine

Kranich

Dringen

Sandberg

et al. 1998

Glia

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Density‐dependent regulation of cell surface γ‐glutamyl transpeptidase in cultured glial cells

Morgenstern¹,

Hanson‐Painton²,

Wang³

et al. 1992

Journal Cellular Physiology

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A decline in cell surface gamma-glutamyl transpeptidase specific activity was previously observed to be concomitant with C6 glial cell proliferation. To elucidate the underlying factor(s) mediating gamma-glutamyl transpeptidase down-regulation, the effects of C6 cell density and culture conditions on cell surface transpeptidase activity levels were investigated. After 24 h of culture, the transpeptidase specific activities were inversely related to the initial plating densities. The lower-density cultures showed an induction within 24 h of plating. As the cultures proliferated, the specific transpeptidase activities declined to a common low level at post-confluency. The gamma-glutamyl transpeptidase down-regulation was unrelated to cell growth rate and was most pronounced during logarithmic proliferation. Induction and down-regulation of gamma-glutamyl transpeptidase activity at low cell densities were not a result of trypsinization. Supplementation of low-density cultures with conditioned medium, use of matrix-coated wells, or periodic replacement of growth media to prevent conditioning had minor effects on the decline of cell surface activity. Kinetic analysis showed that the Michaelis constants and the reaction mechanism were unaltered by cell density, indicating that down-regulation was not due to allosteric factors or an alteration in enzyme character. A reduction in the maximal velocity of cell surface transpeptidation at higher cell densities suggested that gamma-glutamyl transpeptidase down-regulation is related to the concentration of enzyme at the cell surface. Immunocytochemical localization of gamma-glutamyl transpeptidase demonstrated that gamma-glutamyl transpeptidase antigen levels decrease as C6 cell density increases. These results led us to propose that cell-cell contact stimulates the disappearance of gamma-glutamyl transpeptidase from the surface of cultured C6 glial cells.

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Changes in the activity of γ-glutamyl transpeptidase in brain microvessels, astroglial cells and synaptosomes derived from rats with hepatic encephalopathy

Cited by 27 publications

References 23 publications

Alterations of Blood Brain Barrier Function in Hyperammonemia: An Overview

Alterations of Blood Brain Barrier Function in Hyperammonemia: An Overview

Utilization of cysteine and cysteine precursors for the synthesis of glutathione in astroglial cultures: Preference for cystine

Density‐dependent regulation of cell surface γ‐glutamyl transpeptidase in cultured glial cells

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