Potentiation of lead-induced cell death in PC12 cells by glutamate: protection by N-acetylcysteine amide (NACA), a novel thiol antioxidant.

[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 .