Potentiation of lead-induced cell death in PC12 cells by glutamate: protection by N-acetylcysteine amide (NACA), a novel thiol antioxidant.
暂无分享,去创建一个
W. Banks | N. Ercal | S. Penugonda | Suneetha Mare | P. Lutz
[1] L. Strużyńska,et al. Changes in expression of neuronal and glial glutamate transporters in lead-exposed adult rat brain , 2005, Neurochemistry International.
[2] W. Banks,et al. Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12 , 2005, Brain Research.
[3] N. Aykin-Burns,et al. Effects of N-Acetylcysteine on Lead-Exposed PC-12 Cells , 2005, Archives of environmental contamination and toxicology.
[4] E. Melamed,et al. A low molecular weight copper chelator crosses the blood–brain barrier and attenuates experimental autoimmune encephalomyelitis , 2004, Journal of neurochemistry.
[5] Guoyao Wu,et al. Glutathione metabolism and its implications for health. , 2004, The Journal of nutrition.
[6] K. Vähäkangas,et al. Glutamate increases toxicity of inorganic lead in GT1-7 neurons: partial protection induced by flunarizine , 2003, Archives of Toxicology.
[7] D. Cory-Slechta. Lead-Induced Impairments in Complex Cognitive Function: Offerings from Experimental Studies , 2003, Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence.
[8] H. Gurer,et al. Antioxidant Effect of Taurine Against Lead-Induced Oxidative Stress , 2001, Archives of environmental contamination and toxicology.
[9] E. Marra,et al. Glutamate neurotoxicity, oxidative stress and mitochondria , 2001, FEBS letters.
[10] M. Gilbert,et al. Rat hippocampal NMDA receptor binding as a function of chronic lead exposure level. , 2001, Neurotoxicology and teratology.
[11] S. Lasley,et al. Glutamatergic components underlying lead-induced impairments in hippocampal synaptic plasticity. , 2000, Neurotoxicology.
[12] H. Gurer,et al. Can antioxidants be beneficial in the treatment of lead poisoning? , 2000, Free radical biology & medicine.
[13] S. Orrenius,et al. Triggering and modulation of apoptosis by oxidative stress. , 2000, Free radical biology & medicine.
[14] C. Oliveira,et al. Oxidative glutamate toxicity involves mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis , 2000, Neuroscience Research.
[15] G. Ramesh,et al. Contribution of protein kinase C and glutamate in Pb(2+)-induced cytotoxicity. , 2000, Toxicology letters.
[16] C. Culmsee,et al. Cellular and Molecular Mechanisms Underlying Perturbed Energy Metabolism and Neuronal Degeneration in Alzheimer's and Parkinson's Diseases , 1999, Annals of the New York Academy of Sciences.
[17] J. Joseph,et al. Quantifying cellular oxidative stress by dichlorofluorescein assay using microplate reader. , 1999, Free radical biology & medicine.
[18] H. Gurer,et al. Antioxidant role of α-lipoic acid in lead toxicity , 1999 .
[19] G. Goldstein,et al. Molecular Mechanisms of Lead Neurotoxicity , 1999, Neurochemical Research.
[20] B. Yu,et al. Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake. , 1999, Free radical biology & medicine.
[21] H. Gurer,et al. Captopril as an antioxidant in lead-exposed Fischer 344 rats , 1999, Human & experimental toxicology.
[22] Keisuke Kuida,et al. Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9 , 1998, Cell.
[23] K. Savolainen,et al. Glutamate-stimulated ROS production in neuronal cultures: interactions with lead and the cholinergic system. , 1998, Neurotoxicology.
[24] Xiaodong Wang,et al. Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c , 1996, Cell.
[25] D. Duval,et al. Cytotoxic effects of an oxidative stress on neuronal-like pheochromocytoma cells (PC12). , 1996, Biochemical pharmacology.
[26] K. Savolainen,et al. Amplification of glutamate-induced oxidative stress. , 1995, Toxicology Letters.
[27] K. Savolainen,et al. Lead amplifies glutamate-induced oxidative stress. , 1995, Free radical biology & medicine.
[28] G. Benzi,et al. Age- and peroxidative stress-related modifications of the cerebral enzymatic activities linked to mitochondria and the glutathione system. , 1995, Free radical biology & medicine.
[29] R. Burke,et al. 6-Hydroxydopamine lesion of the rat substantia nigra: time course and morphology of cell death. , 1995, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.
[30] D. Spitz,et al. Analysis of glutathione, glutathione disulfide, cysteine, homocysteine, and other biological thiols by high-performance liquid chromatography following derivatization by n-(1-pyrenyl)maleimide. , 1995, Analytical biochemistry.
[31] K. Tipton,et al. Alteration in the glial cell metabolism of glutamate by kainate and N-methyl-D-aspartate. , 1995, Toxicon : official journal of the International Society on Toxinology.
[32] J. Coyle,et al. Oxidative stress, glutamate, and neurodegenerative disorders. , 1993, Science.
[33] E. Squires,et al. A comparative evaluation of thiobarbituric acid methods for the determination of malondialdehyde in biological materials. , 1993, Free radical biology & medicine.
[34] B. Hyman,et al. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[35] E. Silbergeld. Mechanisms of lead neurotoxicity, or looking beyond the lamppost , 1992, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[36] Li Chen,et al. Protein kinase C reduces Mg2+ block of NMDA-receptor channels as a mechanism of modulation , 1992, Nature.
[37] J. G. Cory,et al. Use of an aqueous soluble tetrazolium/formazan assay for cell growth assays in culture. , 1991, Cancer communications.
[38] G. Goldstein,et al. Mechanisms of lead neurotoxicity. , 1991, Biochemical pharmacology.
[39] J. Volpe,et al. Glutamine synthetase activity of developing astrocytes is inhibited in vitro by very low concentrations of lead. , 1990, Brain research. Developmental brain research.
[40] T. Murphy,et al. Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress , 1989, Neuron.
[41] J. Nicolas,et al. Chemiluminescent assay of lipid hydroperoxides. , 1988, Journal of bioluminescence and chemiluminescence.
[42] M. Mayer,et al. Permeation and block of N‐methyl‐D‐aspartic acid receptor channels by divalent cations in mouse cultured central neurones. , 1987, The Journal of physiology.
[43] J. Olson,et al. Lead toxicity in primary cultured cerebral astrocytes and cerebellar granular neurons. , 1987, Toxicology and applied pharmacology.
[44] H. Onoe,et al. Assay of phospholipase A2 activity of synaptic membranes using a phospholipid transfer protein: stimulation by depolarization. , 1986, Biochimica et biophysica acta.
[45] M. M. Bradford. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.
[46] E. Stadtman,et al. Regulation of glutamine synthetase. XI. The nature and implications of a lag phase in the Escherichia coli glutamine synthetase reaction. , 1968, Biochemistry.
[47] D. Atlas,et al. N-acetylcysteine amide, a novel cell-permeating thiol, restores cellular glutathione and protects human red blood cells from oxidative stress. , 2005, Free radical biology & medicine.
[48] J. Clark,et al. Deoletion of brain glutathione is accompanied by impaired micochondrial function and decreased N-acetyl aspartate concentration , 2004, Neurochemical Research.
[49] J. Schneider,et al. Lead neurotoxicity in children: basic mechanisms and clinical correlates. , 2003, Brain : a journal of neurology.
[50] Guangjun Nie,et al. Distinct effects of tea catechins on 6-hydroxydopamine-induced apoptosis in PC12 cells. , 2002, Archives of biochemistry and biophysics.
[51] H. Gurer,et al. Antioxidant role of alpha-lipoic acid in lead toxicity. , 1999, Free radical biology & medicine.
[52] D. Spitz,et al. In vivo indices of oxidative stress in lead-exposed C57BL/6 mice are reduced by treatment with meso-2,3-dimercaptosuccinic acid or N-acetylcysteine. , 1996, Free radical biology & medicine.
[53] T. Simons. Lead-calcium interactions in cellular lead toxicity. , 1993, Neurotoxicology.
[54] E. Tiffany-Castiglioni,et al. Reduction of glutamine synthetase activity in astroglia exposed in culture to low levels of inorganic lead. , 1991, Toxicology.
[55] D. Janero,et al. Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury. , 1990, Free radical biology & medicine.
[56] J. Olson,et al. Maturation of resistance to lead encephalopathy: cellular and subcellular mechanisms. , 1984, Neurotoxicology.
[57] Gary R. Mirams,et al. Toxicology and Applied Pharmacology , 1959, Nature.
[58] Short Communication Mediators of Inflammation, 10, 37–41 (2001) , 2022 .