Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats

Wysmyk, Urszula; Oja, Simo S.; Saransaari, Pirjo

doi:10.1007/bf03160995

Molecular and Chemical Neuropathology

1991

DOI: 10.1007/bf03160995

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Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats

Urszula Wysmyk

Simo S. Oja

Pirjo Saransaari

Abstract: The possible involvement of taurine in the pathogenesis of hepatic encephalopathy was studied in rats injected with thioacetamide. Spontaneous release of exogenous labeled taurine was not affected in any brain area studied, but the potassium-stimulated release was enhanced in the striatum in thioacetamide-treated rats. High concentrations of ammonium ions also evoked greater release of taurine from striatal slices in rats with thioacetamide-induced hepatic encephalopathy.

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Cited by 5 publications

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“…HA or HE are often associated with brain edema resulting primarily from ammonia-induced swelling of astrocytes (Ede and Williams, 1984;Ganz et al, 1989;Norenberg et al, 1991). Also, either HE or HA in different models was found to be accompanied by changes in blood and brain Tau content (Zimmermann et al, 1989;Maddison et al, 1990;Bosman et al, 1992;Hilgier and Olson, 1994), including its distribution between the intracellular and extracellular space of the brain (Bosman et al, 1992), and in depolarization induced Tau release from brain slices (Wysmyk et al, 1991). However, the magnitude and direction of the changes differed with the models and brain regions, and the relative contribution of different factors determining Tau distribution has not been evaluated in detail.…”

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confidence: 99%

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

1996

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Taurine (Tau), an amino acid that abounds in brain, has been implicated in inhibitory neuromodulation and osmoregulation, the latter function being manifested by Tau release along with osmotically obligated water in response to brain tissue edema. A previous study (Hilgier and Olson: J. Neurochem. 62:197–204, 1994) had shown that simple hyperammonemia (HA) induced in rats by daily administration of ammonium acetate resulted in a decrease of both tissue specific gravity indicative of edema and Tau content, in basal ganglia (BG) but not in cerebral cortex (CC). By contrast, rats with hepatic encephalopathy (HE) following administration of a hepatotoxin, thioacetamide, were characterized by CC edema and an increased Tau content in both BG and CC. In the present study, we tested the following parameters that may potentially have affected Tau distribution in the two models: a) spontaneous, and stimulated (hypoosmolarity‐induced) release of loaded [3H] Tau in vitro from CC and BG slices; b) blood Tau content; and c) uptake of [14C] Tau in vivo from blood to brain corrected for [3H] water passage—the so‐called brain uptake index (BUI). The two edema‐affected structures: BG in the HA model and CC in the HE model, showed increased spontaneous Tau release. Edema‐associated spontaneous release of Tau may favor inhibitory neurotransmission contributing to the pathomechanism of HA or HE. Stimulated release, reflecting the ability of the tissue to reduce water content, was decreased in the BG from HA rats, in agreement with the postulated role of Tau in osmoregulation. Stimulated release was unchanged in CC of HE rats. Neither spontaneous nor stimulated release of Tau were affected in CC of HA rats or in BG of HE rats. HE, but not HA, was associated with elevated blood content and increased BUI for TAU, which in combination, contributed to the increase of Tau content in CC. The latter phenomenon adds to the list of metabolic changes distinguishing simple HA from toxic liver damage, reemphasizing the crucial role of factors other than ammonia in the pathomechanism of HE. © 1996 Wiley‐Liss, Inc.

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Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

1996

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Enhanced GABA release in cerebral cortical slices derived from rats with thioacetamide-induced hepatic encephalopathy

et al. 1992

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The release of newly loaded [3H]GABA was studied in slices of different brain regions derived from rats in which acute hepatic encephalopathy (HE) was induced with a hepatotoxin thioacetamide. HE increased both spontaneous and high (50 mM) ammonium chloride-evoked GABA release in cerebral cortical slices by 38% and 50%, respectively. No effects of HE were noted in cerebellar or striatal slices. An increased release of GABA in the cerebral cortex may contribute to the endogenous benzodiazepine-mediated enhancement of GABAergic tone, which is thought to be partly responsible for the pathophysiological mechanism of HE.

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Taurine and neural cell damage

Saransaari¹,

Oja²

2000

Amino Acids

223

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The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia, free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl- channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release may modify neuronal excitability in hyperammonic conditions. Taurine released simultane ously with an excess of excitatory amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may prevent excitation from reaching neurotoxic levels.

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Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats

Cited by 5 publications

References 42 publications

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

Enhanced GABA release in cerebral cortical slices derived from rats with thioacetamide-induced hepatic encephalopathy

Taurine and neural cell damage

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