Role of reactive oxygen species in the neurotoxicity of environmental agents implicated in Parkinson's disease.

No abstract is available for this paper.

• Publication year

  2008

• Venue

  Free Radical Biology & Medicine

• Publication date

  2008-06-01

• Fields of study

  Biology, Medicine, Environmental Science

• Identifiers
  DOI 10.1016/j.freeradbiomed.2008.02.008PMID 18342017PMCID PMC2723777
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• [Parkinson's disease].

  2022cited by this paper
• Dithiocarbamates and the redox regulation of cell death

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• Oxidative Stress in Parkinson's Disease

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• Complex I Is the Major Site of Mitochondrial Superoxide Production by Paraquat*

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• Dieldrin elicits a widespread DNA repair and antioxidative response in mouse brain

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• Nonsteroidal Anti-Inflammatory Drugs and the Risk of Parkinson Disease

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• Paraquat Increases Cyanide-insensitive Respiration in Murine Lung Epithelial Cells by Activating an NAD(P)H:Paraquat Oxidoreductase

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• Parkinson's disease.

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• Induction of microglial reactive oxygen species production by the organochlorinated pesticide dieldrin.

  2007cited by this paper
• Mechanism of toxicity of pesticides acting at complex I: relevance to environmental etiologies of Parkinson’s disease

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• DJ-1 and Parkin modulate dopamine-dependent behavior and inhibit MPTP-induced nigral dopamine neuron loss in mice.

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• Microglial activation as a priming event leading to paraquat-induced dopaminergic cell degeneration.

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• Reactive oxygen species generation by the ethylene-bis-dithiocarbamate (EBDC) fungicide mancozeb and its contribution to neuronal toxicity in mesencephalic cells.

  2007cited by this paper
• Non-motor dysfunction in Parkinson's disease.

  2007cited by this paper
• DJ-1 and Parkin Modulate Dopamine-dependent Behavior and Inhibit MPTP-induced Nigral Dopamine Neuron Loss in Mice.

  2007cited by this paper
• Mitochondria Are a Major Source of Paraquat-induced Reactive Oxygen Species Production in the Brain*

  2007influential reference
• An Orally Active Catalytic Metalloporphyrin Protects against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Neurotoxicity In Vivo

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• Dieldrin exposure induces oxidative damage in the mouse nigrostriatal dopamine system.

  2007cited by this paper
• Parkinsonism genes: culprits and clues

  2006influential reference
• PARK7 DJ-1 protects against degeneration of nigral dopaminergic neurons in Parkinson's disease rat model.

  2006cited by this paper
• Parkinson's disease and pesticide exposures.

  2006cited by this paper
• Acute neurotoxic effects of mancozeb and maneb in mesencephalic neuronal cultures are associated with mitochondrial dysfunction.

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• Developmental exposure to the pesticide dieldrin alters the dopamine system and increases neurotoxicity in an animal model of Parkinson's disease

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• DJ-1, a cancer- and Parkinson's disease-associated protein, stabilizes the antioxidant transcriptional master regulator Nrf2

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• Wild-type PINK1 Prevents Basal and Induced Neuronal Apoptosis, a Protective Effect Abrogated by Parkinson Disease-related Mutations*

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• Pesticides and Parkinson’s Disease—Is There a Link?

  2005cited by this paper
• Dieldrin Induces Ubiquitin-Proteasome Dysfunction in α-Synuclein Overexpressing Dopaminergic Neuronal Cells and Enhances Susceptibility to Apoptotic Cell Death

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• Paraquat neurotoxicity is distinct from that of MPTP and rotenone.

  2005cited by this paper
• Modulation of antioxidant defense systems by the environmental pesticide maneb in dopaminergic cells.

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• Manganese Superoxide Dismutase Protects against 6-Hydroxydopamine Injury in Mouse Brains*

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• Role of mitochondria in toxic oxidative stress.

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• Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stability.

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• Toxin-induced models of Parkinson’s disease

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• Superoxide Dismutase/Catalase Mimetics Are Neuroprotective against Selective Paraquat-mediated Dopaminergic Neuron Death in the Substantial Nigra

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• Overexpression of Superoxide Dismutase or Glutathione Peroxidase Protects against the Paraquat + Maneb-induced Parkinson Disease Phenotype*

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• Dieldrin-induced neurotoxicity: relevance to Parkinson's disease pathogenesis.

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• Role of oxidative stress in paraquat‐induced dopaminergic cell degeneration

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• Iron dysregulation and Parkinson's disease

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• Mitochondrial localization of the Parkinson's disease related protein DJ-1: implications for pathogenesis.

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• Reactive Oxygen and Nitrogen Species: Weapons of Neuronal Destruction in Models of Parkinson's Disease

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• The Role of Microglia in Paraquat-Induced Dopaminergic Neurotoxicity

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• Characterization of Superoxide-producing Sites in Isolated Brain Mitochondria*

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• DJ‐1 has a role in antioxidative stress to prevent cell death

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• Neurodegenerative diseases and oxidative stress

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• No evidence for heritability of Parkinson disease in Swedish twins

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• Parkinson's Disease Mechanisms and Models

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• Mechanism of Toxicity in Rotenone Models of Parkinson's Disease

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• Production of Reactive Oxygen Species by Mitochondria

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• Dieldrin induces apoptosis by promoting caspase-3-dependent proteolytic cleavage of protein kinase Cdelta in dopaminergic cells: relevance to oxidative stress and dopaminergic degeneration.

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• Caspase‐3 dependent proteolytic activation of protein kinase Cδ mediates and regulates 1‐methyl‐4‐phenylpyridinium (MPP+)‐induced apoptotic cell death in dopaminergic cells: relevance to oxidative stress in dopaminergic degeneration

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• Dopamine is involved in selectivity of dopaminergic neuronal death by rotenone

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• Paraquat leads to dopaminergic neural vulnerability in organotypic midbrain culture.

  2003influential reference
• Nonsteroidal anti-inflammatory drugs and the risk of Parkinson disease.

  2003cited by this paper
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  2003cited by this paper
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  2003influential reference
• Cyclooxygenase-2 is instrumental in Parkinson's disease neurodegeneration

  2003influential reference
• The environment and Parkinson's disease: is the nigrostriatal system preferentially targeted by neurotoxins?

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