ReviewAntioxidants (Basel, Switzerland)2022
Neuroprotection against Aminochrome Neurotoxicity: Glutathione Transferase M2-2 and DT-Diaphorase.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Aminochrome-Induced Disruption of Autophagosome-Lysosome Fusion: Implications for Protein Aggregation in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Dopamine-Derived Oxidative Stress in Attention-Deficit/Hyperactivity Disorder: A Narrative Review of Molecular Mechanisms, Neural Circuitry, and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Lactoperoxidase is a candidate for mediating neuromelanin formation in the human substantia nigra.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The conundrum of alpha-synuclein antibody failures in Parkinson's disease: a narrative review of mechanisms and alternative metabolic hypotheses.Therapeutic advances in neurological disorders · 2026Review
- Neuromelanin-induced cellular stress and neurotoxicity in the pathogenesis of Parkinson's disease.Apoptosis : an international journal on programmed cell death · 2025Review
- A Potential Role of Natural Bioactive Compounds Found in Food in the Prevention of Idiopathic Parkinson's Disease.Nutrients · 2025Review
- Natural Compounds That Activate the KEAP1/Nrf2 Signaling Pathway as Potential New Drugs in the Treatment of Idiopathic Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Targets to Search for New Pharmacological Treatment in Idiopathic Parkinson's Disease According to the Single-Neuron Degeneration Model.Biomolecules · 2024Review
- Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson's Disease.Cells · 2024Review
- Single-neuron neurodegeneration as a degenerative model for Parkinson's disease.Neural regeneration research · 2024Review
- Metabolic energy decline coupled dysregulation of catecholamine metabolism in physiologically highly active neurons: implications for selective neuronal death in Parkinson's disease.Frontiers in aging neuroscience · 2024Article
- On the Role of Iron in Idiopathic Parkinson's Disease.Biomedicines · 2023Review
- Why are neuromelanin-containing dopaminergic neurons lost in idiopathic Parkinson's disease?Cellular and molecular life sciences : CMLS · 2023Article
- Protective Effects of Flavonoid Rutin Against Aminochrome Neurotoxicity.Neurotoxicity research · 2023Article
- A Preclinical Model for Parkinson's Disease Based on Transcriptional Gene Activation via KEAP1/NRF2 to Develop New Antioxidant Therapies.Antioxidants (Basel, Switzerland) · 2023Review
- In vivo reduction of age-dependent neuromelanin accumulation mitigates features of Parkinson's disease.Brain : a journal of neurology · 2023Article
- Astrocyte metabolism and signaling pathways in the CNS.Frontiers in neuroscience · 2023Review
- Neuroprotective Capability of Narcissoside in 6-OHDA-Exposed Parkinson's Disease Models through Enhancing the MiR200a/Nrf-2/GSH Axis and Mediating MAPK/Akt Associated Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Glutathione is an important antioxidant that plays a crucial role in the cellular protection against oxidative stress and detoxification of electrophilic mutagens, and carcinogens. Glutathione transferases are enzymes catalyzing glutathione-dependent reactions that lead to inactivation and conjugation of toxic compounds, processes followed by subsequent excretion of the detoxified products. Degeneration and loss of neuromelanin-containing dopaminergic neurons in the nigrostriatal neurons generally involves oxidative stress, neuroinflammation, alpha-synuclein aggregation to neurotoxic oligomers, mitochondrial dysfunction, protein degradation dysfunction, and endoplasmic reticulum stress. However, it is still unclear what triggers these neurodegenerative processes. It has been reported that aminochrome may elicit all of these mechanisms and, interestingly, aminochrome is formed inside neuromelanin-containing dopaminergic neurons during neuromelanin synthesis. Aminochrome is a neurotoxic ortho-quinone formed in neuromelanin synthesis. However, it seems paradoxical that the neurotoxin aminochrome is generated during neuromelanin synthesis, even though healthy seniors have these neurons intact when they die. The explanation of this paradox is the existence of protective tools against aminochrome neurotoxicity composed of the enzymes DT-diaphorase, expressed in these neurons, and glutathione transferase M2-2, expressed in astrocytes. Recently, it has been reported that dopaminergic neurons can be protected by glutathione transferase M2-2 from astrocytes, which secrete exosomes containing the protective enzyme.
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Registered trials
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