ArticleNeurotoxicity research2016
Aminochrome Toxicity is Mediated by Inhibition of Microtubules Polymerization Through the Formation of Adducts with Tubulin.
Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Aminochrome-Induced Disruption of Autophagosome-Lysosome Fusion: Implications for Protein Aggregation in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Nicotine protects astrocytes expressing alpha-synuclein against aminochrome cytotoxicity: Implications for Parkinson's disease.Research square · 2026Article
- Targets to Search for New Pharmacological Treatment in Idiopathic Parkinson's Disease According to the Single-Neuron Degeneration Model.Biomolecules · 2024Review
- 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
- Aminochrome Induces Neuroinflammation and Dopaminergic Neuronal Loss: A New Preclinical Model to Find Anti-inflammatory and Neuroprotective Drugs for Parkinson's Disease.Cellular and molecular neurobiology · 2023Article
- The diverse functionality of NQO1 and its roles in redox control.Redox biology · 2021Review
- The Effect of Oxidized Dopamine on the Structure and Molecular Chaperone Function of the Small Heat-Shock Proteins, αB-Crystallin and Hsp27.International journal of molecular sciences · 2021Article
- Cellular Trafficking of Glutathione Transferase M2-2 Between U373MG and SHSY-S7 Cells is Mediated by Exosomes.Neurotoxicity research · 2021Article
- The Flavonoid Agathisflavone from Poincianella pyramidalis Prevents Aminochrome Neurotoxicity.Neurotoxicity research · 2020Article
- Novel Alpha-Synuclein Oligomers Formed with the Aminochrome-Glutathione Conjugate Are Not Neurotoxic.Neurotoxicity research · 2019Article
- Overexpression of Vesicular Monoamine Transporter-2 may Block Neurotoxic Metabolites from Cytosolic Dopamine: a Potential Neuroprotective Therapy for Parkinson's Disease.Clinical pharmacology and translational medicine · 2019Article
- On the Role of Aminochrome in Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Parkinson's Disease.Frontiers in neuroscience · 2019Article
- Neurotoxins as Preclinical Models for Parkinson's Disease.Neurotoxicity research · 2018Review
- Covalent binding of the organophosphate insecticide profenofos to tyrosine on α- and β-tubulin proteins.Chemosphere · 2018Article
- On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease.Neural regeneration research · 2017Review
- Aminochrome induces dopaminergic neuronal dysfunction: a new animal model for Parkinson's disease.Cellular and molecular life sciences : CMLS · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the role of adducts formation between aminochrome and tubulin and its interference in microtubules assembly and stability in aminochrome-induced toxicity in SH-SY5Y cells. We also investigated whether changes in the microtubules structures are an early event that could affect tubulin expression. We demonstrated in vitro that aminochrome tubulin adducts inhibit tubulin polymerization and that aminochrome induces microtubules disassembly. Moreover, when the SH-SY5Y cells were incubated with aminochrome, we observed an increase in soluble tubulin, indicating depolymerization of microtubules. Aminochrome generates disruption of the microtubules network, leading to changes in the morphology of the cells inducing cell death, in a dose- and time-dependent manner. Interestingly, these changes preceded cell death and were partly inhibited by paclitaxel, a microtubule-stabilizing agent. Furthermore, we observed that aminochrome increased early tubulin expression before significant cell death occurred. Consequently, all these antecedents suggest that aminochrome toxicity is mediated by early disruption of microtubules network, where the adduct formation between aminochrome and tubulin could be responsible for the inhibition in the assembly microtubules and the loss of microtubules stability. Possibly, the early changes in tubulin expression could correspond to compensatory mechanisms against the toxic effects of aminochrome.
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