ArticleMolecular neurodegeneration2011
6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death.
Article in Molecular neurodegeneration, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 91 citations in OpenAlex.
- NDST3-Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- OTUD6A drives dopaminergic neuronal degeneration of Parkinson's disease through deubiquitinating ACTG1 in neuronal cells.Acta pharmaceutica Sinica. B · 2026Article
- Neuroprotective Effects of Thymol-Loaded Selenium Nanoparticles against 6-OHDA-Induced Apoptosis and Oxidative Stress in anCurrent pharmaceutical design · 2026Article
- Targeting the Rho/ROCK Signaling Pathway Mitigates Mitochondrial Dysfunction in 6-OHDA-Induced Models of Parkinson's Disease, Both In Vivo and In Vitro.Molecular neurobiology · 2025Article
- Osteoprotective Effects of Melatonin on Bone Loss Associated with Dopaminergic Neuron Degeneration in a Rat Model of Parkinson Disease.Calcified tissue international · 2025Article
- Co-treatment Strategy Supports Neuroprotection by Intersecting p62-Keap1-NRF2 and Autophagy Signaling Pathways in the Cellular Model of Parkinson's Disease.Cellular and molecular neurobiology · 2025Article
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- Tyrosinase-induced neuromelanin accumulation triggers rapid dysregulation and degeneration of the mouse locus coeruleus.bioRxiv : the preprint server for biology · 2025Article
- Robust In Vitro Models for Studying Parkinson's Disease? LUHMES Cells and SH-SH5Y Cells.International journal of molecular sciences · 2024Article
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- Effectiveness of Albumin-Fused Thioredoxin against 6-Hydroxydopamine-Induced Neurotoxicity In Vitro.International journal of molecular sciences · 2023Article
- Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.Translational neurodegeneration · 2023Review
- DNA Damage-Mediated Neurotoxicity in Parkinson's Disease.International journal of molecular sciences · 2023Review
- IDO1 Modulates the Sensitivity of Epithelial Ovarian Cancer Cells to Cisplatin through ROS/p53-Dependent Apoptosis.International journal of molecular sciences · 2022Article
- Omarigliptin Mitigates 6-Hydroxydopamine- or Rotenone-Induced Oxidative Toxicity in PC12 Cells by Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Actions.Antioxidants (Basel, Switzerland) · 2022Article
- α-synucleinopathy exerts sex-dimorphic effects on the multipurpose DNA repair/redox protein APE1 in mice and humans.Progress in neurobiology · 2022Article
- Galangin Exhibits Neuroprotective Effects in 6-OHDA-Induced Models of Parkinson's Disease via the Nrf2/Keap1 Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The Complex Mechanisms by Which Neurons Die Following DNA Damage in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Cerebrospinal Fluid Metabolome in Parkinson's Disease and Multiple System Atrophy.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundParkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN), resulting in tremor, rigidity, and bradykinesia. Although the etiology is unknown, insight into the disease process comes from the dopamine (DA) derivative, 6-hydroxydopamine (6-OHDA), which produces PD-like symptoms. Studies show that 6-OHDA activates stress pathways, such as the unfolded protein response (UPR), triggers mitochondrial release of cytochrome-c, and activates caspases, such as caspase-3. Because the BH3-only protein, Puma (p53-upregulated mediator of apoptosis), is activated in response to UPR, it is thought to be a link between cell stress and apoptosis.
resultsTo test the hypothesis that Puma serves such a role in 6-OHDA-mediated cell death, we compared the response of dopaminergic neurons from wild-type and Puma-null mice to 6-OHDA. Results indicate that Puma is required for 6-OHDA-induced cell death, in primary dissociated midbrain cultures as well as in vivo. In these cultures, 6-OHDA-induced DNA damage and p53 were required for 6-OHDA-induced cell death. In contrast, while 6-OHDA led to upregulation of UPR markers, loss of ATF3 did not protect against 6-OHDA.
conclusionsTogether, our results indicate that 6-OHDA-induced upregulation of Puma and cell death are independent of UPR. Instead, p53 and DNA damage repair pathways mediate 6-OHDA-induced toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.