The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

Michael Aschner - One of the best experts on this subject based on the ideXlab platform.

  • adenosine modulates Methylmercuric Chloride mehgcl inducedd aspartate release from neonatal rat primary astrocyte cultures
    Brain Research, 1995
    Co-Authors: Michael Aschner, K J Mullaney, D E Wagoner, Lawrence H Lash, Harold K Kimelberg
    Abstract:

    Abstract The effects of adenosine, and selective adenosine receptor agonists and antagonists on methylmercury (MeHg)-induced aspartate release were studied in neonatal rat primary astrocyte cultures. Whereas basal levels of d -[3H]aspartate release were unchanged upon treatment with adenosine or selective A1 receptor agonists, N6-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release of d -aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-induced d -[3H]aspartate release. Since the effect of MeHg on d -[3H]aspartate release is known to be associated with sulfhydryl (-SH) groups which are controlled by intracellular glutathione concentrations [GSH]i, we also evaluated the effects of adenosine, the A1 agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH]i. Attenuation of the stimulatory effect of MeHg on d -[3H]aspartate release by adenosine and its agonists occurred in the presence of reduced astrocytic [GSH]i, suggesting that other mechanisms must be invoked for this protective effect. Whilst the mechanism of MeHg-induced d -[3H]aspartate release is not known, the data suggest a role for adenosine in its regulation.

  • the role of sh groups in Methylmercuric Chloride induced d aspartate and rubidium release from rat primary astrocyte cultures
    Brain Research, 1994
    Co-Authors: K J Mullaney, M N Fehm, D Vitarella, D E Wagoner, Michael Aschner
    Abstract:

    Abstract Methylmercuric Chloride (MeHgCl) was shown to increase d -aspartate and rubidium (Rb; a marker for potassium) release from preloaded astrocytes in a dose- and time-dependent fashion. Two sulfhydryl (-SH) protecting agents: a cell membrane non-penetrating compound, reduced glutathione (GSH), and the membrane permeable dithiothreitol (DTT), were found to inhibit the stimulatory action of MeHgCl on the efflux of radiolabeled d -aspartate as well as Rb. MeHgCl-induced d -aspartate and Rb release was completely inhibited by the addition of 1 mM DTT or GSH during the actual 5 min perfusion period with MeHgCl (10 μM). However, when added after MeHgCl treatment, this inhibition could not be fully sustained by GSH, while DTT fully inhibited the MeHgCl-induced release of d -aspartate. Neither DTT or GSH alone had any effect on the rate of astrocytic d -aspartate release. Accordingly, it is postulated that the stimulatory effect exerted by MeHgCl on astrocytic d -aspartate release is associated with vulnerable -SH groups located within, but not on the surface of the cell membrane. Omission of Na + from the perfusion solution did not accelerate MeHgCl-induced d -aspartate release, suggesting that reversal of the d -aspartate carrier cannot be invoked to explain MeHgCl-induced d -aspartate release. Omission of Ca 2+ from the perfusion solution increased the time-dependent MeHgCl-induced d -aspartate release.

K J Mullaney - One of the best experts on this subject based on the ideXlab platform.

  • adenosine modulates Methylmercuric Chloride mehgcl inducedd aspartate release from neonatal rat primary astrocyte cultures
    Brain Research, 1995
    Co-Authors: Michael Aschner, K J Mullaney, D E Wagoner, Lawrence H Lash, Harold K Kimelberg
    Abstract:

    Abstract The effects of adenosine, and selective adenosine receptor agonists and antagonists on methylmercury (MeHg)-induced aspartate release were studied in neonatal rat primary astrocyte cultures. Whereas basal levels of d -[3H]aspartate release were unchanged upon treatment with adenosine or selective A1 receptor agonists, N6-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release of d -aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-induced d -[3H]aspartate release. Since the effect of MeHg on d -[3H]aspartate release is known to be associated with sulfhydryl (-SH) groups which are controlled by intracellular glutathione concentrations [GSH]i, we also evaluated the effects of adenosine, the A1 agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH]i. Attenuation of the stimulatory effect of MeHg on d -[3H]aspartate release by adenosine and its agonists occurred in the presence of reduced astrocytic [GSH]i, suggesting that other mechanisms must be invoked for this protective effect. Whilst the mechanism of MeHg-induced d -[3H]aspartate release is not known, the data suggest a role for adenosine in its regulation.

  • the role of sh groups in Methylmercuric Chloride induced d aspartate and rubidium release from rat primary astrocyte cultures
    Brain Research, 1994
    Co-Authors: K J Mullaney, M N Fehm, D Vitarella, D E Wagoner, Michael Aschner
    Abstract:

    Abstract Methylmercuric Chloride (MeHgCl) was shown to increase d -aspartate and rubidium (Rb; a marker for potassium) release from preloaded astrocytes in a dose- and time-dependent fashion. Two sulfhydryl (-SH) protecting agents: a cell membrane non-penetrating compound, reduced glutathione (GSH), and the membrane permeable dithiothreitol (DTT), were found to inhibit the stimulatory action of MeHgCl on the efflux of radiolabeled d -aspartate as well as Rb. MeHgCl-induced d -aspartate and Rb release was completely inhibited by the addition of 1 mM DTT or GSH during the actual 5 min perfusion period with MeHgCl (10 μM). However, when added after MeHgCl treatment, this inhibition could not be fully sustained by GSH, while DTT fully inhibited the MeHgCl-induced release of d -aspartate. Neither DTT or GSH alone had any effect on the rate of astrocytic d -aspartate release. Accordingly, it is postulated that the stimulatory effect exerted by MeHgCl on astrocytic d -aspartate release is associated with vulnerable -SH groups located within, but not on the surface of the cell membrane. Omission of Na + from the perfusion solution did not accelerate MeHgCl-induced d -aspartate release, suggesting that reversal of the d -aspartate carrier cannot be invoked to explain MeHgCl-induced d -aspartate release. Omission of Ca 2+ from the perfusion solution increased the time-dependent MeHgCl-induced d -aspartate release.

D E Wagoner - One of the best experts on this subject based on the ideXlab platform.

  • adenosine modulates Methylmercuric Chloride mehgcl inducedd aspartate release from neonatal rat primary astrocyte cultures
    Brain Research, 1995
    Co-Authors: Michael Aschner, K J Mullaney, D E Wagoner, Lawrence H Lash, Harold K Kimelberg
    Abstract:

    Abstract The effects of adenosine, and selective adenosine receptor agonists and antagonists on methylmercury (MeHg)-induced aspartate release were studied in neonatal rat primary astrocyte cultures. Whereas basal levels of d -[3H]aspartate release were unchanged upon treatment with adenosine or selective A1 receptor agonists, N6-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release of d -aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-induced d -[3H]aspartate release. Since the effect of MeHg on d -[3H]aspartate release is known to be associated with sulfhydryl (-SH) groups which are controlled by intracellular glutathione concentrations [GSH]i, we also evaluated the effects of adenosine, the A1 agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH]i. Attenuation of the stimulatory effect of MeHg on d -[3H]aspartate release by adenosine and its agonists occurred in the presence of reduced astrocytic [GSH]i, suggesting that other mechanisms must be invoked for this protective effect. Whilst the mechanism of MeHg-induced d -[3H]aspartate release is not known, the data suggest a role for adenosine in its regulation.

  • the role of sh groups in Methylmercuric Chloride induced d aspartate and rubidium release from rat primary astrocyte cultures
    Brain Research, 1994
    Co-Authors: K J Mullaney, M N Fehm, D Vitarella, D E Wagoner, Michael Aschner
    Abstract:

    Abstract Methylmercuric Chloride (MeHgCl) was shown to increase d -aspartate and rubidium (Rb; a marker for potassium) release from preloaded astrocytes in a dose- and time-dependent fashion. Two sulfhydryl (-SH) protecting agents: a cell membrane non-penetrating compound, reduced glutathione (GSH), and the membrane permeable dithiothreitol (DTT), were found to inhibit the stimulatory action of MeHgCl on the efflux of radiolabeled d -aspartate as well as Rb. MeHgCl-induced d -aspartate and Rb release was completely inhibited by the addition of 1 mM DTT or GSH during the actual 5 min perfusion period with MeHgCl (10 μM). However, when added after MeHgCl treatment, this inhibition could not be fully sustained by GSH, while DTT fully inhibited the MeHgCl-induced release of d -aspartate. Neither DTT or GSH alone had any effect on the rate of astrocytic d -aspartate release. Accordingly, it is postulated that the stimulatory effect exerted by MeHgCl on astrocytic d -aspartate release is associated with vulnerable -SH groups located within, but not on the surface of the cell membrane. Omission of Na + from the perfusion solution did not accelerate MeHgCl-induced d -aspartate release, suggesting that reversal of the d -aspartate carrier cannot be invoked to explain MeHgCl-induced d -aspartate release. Omission of Ca 2+ from the perfusion solution increased the time-dependent MeHgCl-induced d -aspartate release.

Harold K Kimelberg - One of the best experts on this subject based on the ideXlab platform.

  • adenosine modulates Methylmercuric Chloride mehgcl inducedd aspartate release from neonatal rat primary astrocyte cultures
    Brain Research, 1995
    Co-Authors: Michael Aschner, K J Mullaney, D E Wagoner, Lawrence H Lash, Harold K Kimelberg
    Abstract:

    Abstract The effects of adenosine, and selective adenosine receptor agonists and antagonists on methylmercury (MeHg)-induced aspartate release were studied in neonatal rat primary astrocyte cultures. Whereas basal levels of d -[3H]aspartate release were unchanged upon treatment with adenosine or selective A1 receptor agonists, N6-cyclopentyladenosine (CPA), cyclohexyladenosine (CHA), and R-phenylisopropyladenosine (R-PIA), all partially reversed the MeHg-induced release of d -aspartate. Treatment of astrocytes with the xanthine derivative, theophylline, an adenosine antagonist, reversed the inhibitory effect of adenosine on MeHg-induced d -[3H]aspartate release. Since the effect of MeHg on d -[3H]aspartate release is known to be associated with sulfhydryl (-SH) groups which are controlled by intracellular glutathione concentrations [GSH]i, we also evaluated the effects of adenosine, the A1 agonists CPA and CHP, and the adenosine antagonist, theophylline, on astrocytic [GSH]i. Attenuation of the stimulatory effect of MeHg on d -[3H]aspartate release by adenosine and its agonists occurred in the presence of reduced astrocytic [GSH]i, suggesting that other mechanisms must be invoked for this protective effect. Whilst the mechanism of MeHg-induced d -[3H]aspartate release is not known, the data suggest a role for adenosine in its regulation.

Younghahn Moon - One of the best experts on this subject based on the ideXlab platform.

  • interaction of sodium selenite on neurotoxicity induced by Methylmercuric Chloride
    Journal of Preventive Medicine and Public Health, 1992
    Co-Authors: Junggyun Park, H M Lee, Y Chung, Dongchun Shin, Jaehoon Roh, Younghahn Moon
    Abstract:

    This study was conducted to investigate the mechanism of protective effect by sodium selenite in Methylmercuric Chloride neurotoxicity, increasing intracellular concentration of the neuron. Methylmercuric Chloride of 3mg/kg of body weight was administered simultaneously with sodium selenite of 5mg/kg and pretreatment of sodium selenite via intraperitoneal injection to rats. Also, effect of Methylmercuric Chloride() and sodium selenite() on free intrasynaptosomal concentration were studied using the fluorescent indicator fura -2 in vitro. After the treatment, at 6, 24, and 48 hours later, mercury in the cerebral cortex, liver and kidney tissues, succlnic dehydrogenase activities, adenosin-5'-triphosphate concentration, acetylcholinesterase activities, and intracellular concentration in the cerebral cortex were determined in vivo. Cerebral synaptosomes of rats were incubated with Methylmercuric Chloride and sodium selenite in Hepes buffer for 10 minutes and free intrasynaptosomal concentration were measured with fura-2 in vitro. The results were summarized as follows ; 1. The combined administration of and and pretreatment of according to time significantly more increased in the cerebral cortex and decreased in the liver, kidney mercury concentrations compared to the administration of only. 2. The combined administration of and and pretreatment of increased more succinic dehydrogenase and acetylcholinesterase activities compared to the administration of only. Particularly pretreatment of significantly more compared to the administration of only. The concentration of adenosine-5'-triphosphate in treatment groups revealed a favourable effect compared to the administration of only. 3. Intracellular concentration in administration of only was increased significantly more than control group in all test hours but was increased significantly more at 48 hours only after treatment in combined administration of and and pretreatment of according to time interval more decreased significantly intracellular concentration compared to the administration of only. 4. Free intrasynaptosomal concentration in the combined administration of and was decreased () significantly more than the administration of only. From the above results, the specific dosage of decreased increment of intracellular concentration induced by administration of . These findings suggest the protective mechanism of on the neurotoxicity of .