ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Repair capacity for platinum-DNA adducts determines the severity of cisplatin-induced peripheral neuropathy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 154 citations in OpenAlex.
- Article
- HMGB1 Assists in Overcoming Cisplatin Resistance in Chemoresistant Human Ovarian Cancer Cells.Molecular carcinogenesis · 2026Article
- The deubiquitinase OTUD1 orchestrates cisplatin chemosensitivity of non-small cell lung cancer through destabilizing RAD23B/XPC.Oncogene · 2025Article
- CD163+ macrophages monitor enhanced permeability at the blood-dorsal root ganglion barrier.The Journal of experimental medicine · 2024Article
- Neuroprotective Effects of Trimetazidine against Cisplatin-Induced Peripheral Neuropathy: Involvement of AMPK-Mediated PI3K/mTOR, Nrf2, and NF-Oxidative medicine and cellular longevity · 2024Article
- Ozone in Chemotherapy-Induced Peripheral Neuropathy-Current State of Art, Possibilities, and Perspectives.International journal of molecular sciences · 2023Review
- Integrated Microarray-Based Data Analysis of miRNA Expression Profiles: Identification of Novel Biomarkers of Cisplatin-Resistance in Testicular Germ Cell Tumours.International journal of molecular sciences · 2023Article
- Oxidative DNA Damage and Cisplatin Neurotoxicity Is Exacerbated by Inhibition of OGG1 Glycosylase Activity and APE1 Endonuclease Activity in Sensory Neurons.International journal of molecular sciences · 2022Article
- Review
- Oxidative DNA Damage: A Role in Altering Neuronal Function.Journal of cellular signaling · 2022Article
- Cisplatin Neurotoxicity Targets Specific Subpopulations and KFrontiers in cellular neuroscience · 2022Article
- Alleviation of cisplatin-induced neuropathic pain, neuronal apoptosis, and systemic inflammation in mice by rapamycin.Frontiers in aging neuroscience · 2022Article
- Mechanisms of Chemotherapy-Induced Neurotoxicity.Frontiers in pharmacology · 2022Review
- Considerations for a Reliable In Vitro Model of Chemotherapy-Induced Peripheral Neuropathy.Toxics · 2021Review
- Cisplatin Mouse Models: Treatment, Toxicity and Translatability.Biomedicines · 2021Review
- Modulation of Glutamate Transporter EAAT1 and Inward-Rectifier Potassium Channel KInternational journal of molecular sciences · 2021Article
- The Effect of Curcumin Nanoparticles on Cisplatin-Induced Cardiotoxicity in Male Wistar Albino Rats.Cardiovascular toxicology · 2021Article
- The Role of Nucleotide Excision Repair in Cisplatin-Induced Peripheral Neuropathy: Mechanism, Prevention, and Treatment.International journal of molecular sciences · 2021Review
- APE1/Ref-1 - One Target with Multiple Indications: Emerging Aspects and New Directions.Journal of cellular signaling · 2021Article
- Pantoprazole abrogated cisplatin-induced nephrotoxicity in mice via suppression of inflammation, apoptosis, and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pronounced neurotoxicity of the potent antitumor drug cisplatin frequently results in the onset of peripheral polyneuropathy (PNP), which is assumed to be initially triggered by platination products in the nuclear DNA of affected tissues. To further elucidate the molecular mechanisms, we analyzed in a mouse model the formation and processing of the main cisplatin-induced DNA adduct (guanine-guanine intrastrand cross-link) in distinct neuronal cell types by adduct-specific monoclonal antibodies. Comparison of the adduct kinetics in cisplatin-injected mice either proficient or deficient for nucleotide excision repair (NER) functions revealed the essential role of this DNA repair pathway in protecting differentiated cells of the nervous system from excessive formation of such lesions. Hence, chronic exposure to cisplatin resulted in an accelerated accumulation of unrepaired intrastrand cross-links in neuronal cells of mice with dysfunctional NER. The augmented adduct levels in dorsal root ganglion (DRG) cells of those animals coincided with an earlier onset of PNP-like functional disturbance of their sensory nervous system. Independently from the respective repair phenotype, the amount of persisting DNA cross-links in DRG neurons at a given cumulative dose was significantly correlated to the degree of sensory impairment as measured by electroneurography. Collectively, these findings suggest a new model for the processing of cisplatin adducts in primary neuronal cells and accentuate the crucial role of effectual DNA repair capacity in the target cells for the individual risk of therapy-induced PNP.
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