Paraquat induces oxidative stress and neuronal cell death; neuroprotection by water-soluble Coenzyme Q10.

[1]  S. Pandey,et al.  Oxidative stress and activation of proteasome protease during serum deprivation-induced apoptosis in rat hepatoma cells; inhibition of cell death by melatonin , 2003, Apoptosis.

[2]  M. Hung,et al.  Oxidative stress-induced apoptosis in dividing fibroblasts involves activation of p38 MAP kinase and over-expression of Bax: Resistance of quiescent cells to oxidative stress , 2004, Apoptosis.

[3]  Ó. González-Pérez,et al.  An alpha-lipoic acid–vitamin E mixture reduces post-embolism lipid peroxidation, cerebral infarction, and neurological deficit in rats , 2003, Neuroscience Research.

[4]  E. Richfield,et al.  Age‐related irreversible progressive nigrostriatal dopaminergic neurotoxicity in the paraquat and maneb model of the Parkinson's disease phenotype , 2003, The European journal of neuroscience.

[5]  Ewa Witort,et al.  Coenzyme Q10 Prevents Apoptosis by Inhibiting Mitochondrial Depolarization Independently of Its Free Radical Scavenging Property* , 2003, Journal of Biological Chemistry.

[6]  P. Walker,et al.  Molecular mechanisms of glutamate neurotoxicity in mixed cultures of NT2‐derived neurons and astrocytes: Protective effects of coenzyme Q10 , 2003, Journal of neuroscience research.

[7]  J. Paul Robinson,et al.  Mitochondrial Complex I Inhibitor Rotenone Induces Apoptosis through Enhancing Mitochondrial Reactive Oxygen Species Production* , 2003, The Journal of Biological Chemistry.

[8]  A. Manning-Boğ,et al.  Environmental factors in Parkinson's disease. , 2002, Neurotoxicology.

[9]  J. Langston,et al.  Environmental Risk Factors and Parkinson's Disease: Selective Degeneration of Nigral Dopaminergic Neurons Caused by the Herbicide Paraquat , 2002, Neurobiology of Disease.

[10]  B. Mignotte,et al.  Mitochondrial reactive oxygen species in cell death signaling. , 2002, Biochimie.

[11]  A. Siraki,et al.  Endogenous and endobiotic induced reactive oxygen species formation by isolated hepatocytes. , 2002, Free radical biology & medicine.

[12]  E. Hickey,et al.  Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death. , 2001, Free radical biology & medicine.

[13]  K. Matsubara,et al.  Carrier-mediated processes in blood–brain barrier penetration and neural uptake of paraquat , 2001, Brain Research.

[14]  P. Parvaz,et al.  Thiram-induced cytotoxicity is accompanied by a rapid and drastic oxidation of reduced glutathione with consecutive lipid peroxidation and cell death. , 2001, Toxicology.

[15]  Hui Zhang,et al.  Dopaminergic cell death induced by MPP+, oxidant and specific neurotoxicants shares the common molecular mechanism , 2001, Journal of neurochemistry.

[16]  Yuhui Liu,et al.  Sequential Treatment of SH‐SY5Y Cells with Retinoic Acid and Brain‐Derived Neurotrophic Factor Gives Rise to Fully Differentiated, Neurotrophic Factor‐Dependent, Human Neuron‐Like Cells , 2000, Journal of neurochemistry.

[17]  D. Price New order from neurological disorders , 1999, Nature.

[18]  D. Selkoe,et al.  Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.

[19]  Anders Björklund,et al.  Prospects for new restorative and neuroprotective treatments in Parkinson's disease , 1999, Nature.

[20]  G. Bignami From entropy to Duino , 1999, Nature.

[21]  Sarah Tomlin,et al.  Microtechnology: Laying it on thick , 1999, Nature.

[22]  S. Melov,et al.  Mitochondrial disease in mouse results in increased oxidative stress. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[23]  G. Cappelletti,et al.  APOPTOSIS IN HUMAN LUNG EPITHELIAL CELLS: TRIGGERING BY PARAQUAT AND MODULATION BY ANTIOXIDANTS , 1998, Cell biology international.

[24]  G. Nisticó,et al.  Paraquat: a useful tool for the in vivo study of mechanisms of neuronal cell death. , 1998, Pharmacology & toxicology.

[25]  J. Lazo,et al.  Paraquat-induced phosphatidylserine oxidation and apoptosis are independent of activation of PLA2. , 1998, American journal of physiology. Lung cellular and molecular physiology.

[26]  J. Jeng,et al.  Environmental risk factors and Parkinson's disease , 1997, Neurology.

[27]  J. D. Young,et al.  Cell suicide in health and disease. , 1996, Scientific American.

[28]  Y. C. Chang,et al.  Effects of paraquat on the substantia nigra of the wistar rats: neurochemical, histological, and behavioral studies. , 1996, Toxicology and applied pharmacology.

[29]  P. Nicotera,et al.  Apoptosis: molecular control point in toxicity. , 1994, Toxicology and applied pharmacology.

[30]  F. Jiménez-Jiménez,et al.  Risk‐factors for Parkinson's disease: case‐control study in the province of Cáceres, Spain , 1994, Acta neurologica Scandinavica.

[31]  G. Cerniglia,et al.  Microtiter plate assay for the measurement of glutathione and glutathione disulfide in large numbers of biological samples. , 1990, Analytical biochemistry.

[32]  L. Onyon,et al.  The Epidemiology and Prevention of Paraquat Poisoning , 1987, Human toxicology.

[33]  A. Wyllie,et al.  Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics , 1972, British Journal of Cancer.