ArticleNeurobiology of disease2017
Cisplatin induces mitochondrial deficits in Drosophila larval segmental nerve.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Platinum Accumulation and Antioxidant Dysregulation Drive Behavioral Impairments, Apoptosis and Neurodegeneration in Oxaliplatin Exposed Drosophila Melanogaster.Biological trace element research · 2026Article
- Preventing neuropathy and improving anticancer chemotherapy with a carbazole-based compound.Science advances · 2025Article
- Isolation of Intact Mitochondria FromBio-protocol · 2025Article
- Review
- 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
- Genetic Reduction of Mitochondria Complex I Subunits is Protective against Cisplatin-Induced Neurotoxicity inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Biological Application of Novel Biodegradable Cellulose Composite as a Hemostatic Material.Mediators of inflammation · 2022Article
- Cellular Pathogenesis of Chemotherapy-Induced Peripheral Neuropathy: Insights FromFrontiers in pain research (Lausanne, Switzerland) · 2022Review
- Oxaliplatin-induced peripheral neuropathy: clinical features, mechanisms, prevention and treatment.Journal of neurology · 2021Review
- Mini-Review: Mitochondrial dysfunction and chemotherapy-induced neuropathic pain.Neuroscience letters · 2021Review
- Early Physiological and Cellular Indicators of Cisplatin-Induced Ototoxicity.Journal of the Association for Research in Otolaryngology : JARO · 2021Article
- Application Potential of Plant-Derived Medicines in Prevention and Treatment of Platinum-Induced Peripheral Neurotoxicity.Frontiers in pharmacology · 2021Review
- Platinum-Induced Peripheral Neuropathy (PIPN): ROS-Related Mechanism, Therapeutic Agents, and Nanosystems.Frontiers in molecular biosciences · 2021Review
- Insights into platinum-induced peripheral neuropathy-current perspective.Neural regeneration research · 2020Review
- Dexmedetomidine attenuates cisplatin-induced cognitive impairment by modulating miR-429-3p expression in rats.3 Biotech · 2020Article
- Analyzing chemotherapy-induced peripheral neuropathy in vivo using non-mammalian animal models.Experimental neurology · 2020Review
- PTEN-Induced Putative Kinase 1 (PINK1)/Parkin-Mediated Mitophagy Protects PC12 Cells Against Cisplatin-Induced Neurotoxicity.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Article
- Platinum-induced neurotoxicity: A review of possible mechanisms.World journal of clinical oncology · 2017Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Cisplatin is an effective chemotherapy drug that induces peripheral neuropathy in cancer patients. In rodent dorsal root ganglion neurons, cisplatin binds nuclear and mitochondrial DNA (mtDNA) inducing DNA damage and apoptosis. Platinum-mtDNA adducts inhibit mtDNA replication and transcription leading to mitochondrial degradation. Cisplatin also induces climbing deficiencies associated with neuronal apoptosis in adult Drosophila melanogaster. Here we used Drosophila larvae that express green fluorescent protein in the mitochondria of motor neurons to observe the effects of cisplatin on mitochondrial dynamics and function. Larvae treated with 10μg/ml cisplatin had normal survival with deficiencies in righting and heat sensing behavior. Behavior was abrogated by, the pan caspase inhibitor, p35. However, active caspase 3 was not detected by immunostaining. There was a 27% decrease in mitochondrial membrane potential and a 42% increase in reactive oxygen species (ROS) in mitochondria along the axon. Examination of mitochondrial axonal trafficking showed no changes in velocity, flux or mitochondrial length. However, cisplatin treatment resulted in a greater number of stationary organelles caused by extended pausing during axonal motility. These results demonstrate that cisplatin induces behavior deficiencies in Drosophila larvae, decreased mitochondrial activity, increased ROS production and mitochondrial pausing without killing the larvae. Thus, we identified particular aspects of mitochondrial dynamics and function that are affected in cisplatin-induced peripheral neuropathy and may represent key therapeutic targets.
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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.