ArticleJournal of toxicology2011
Oxidative toxicity in neurodegenerative diseases: role of mitochondrial dysfunction and therapeutic strategies.
Article in Journal of toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 116 citations in OpenAlex.
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- The Impact of the Delivery Method on Oxidative Stress in Neonates: A Cross-Sectional Study.Journal of clinical medicine · 2025Article
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- Potential Neurotoxic Effects of Glioblastoma-Derived Exosomes in Primary Cultures of Cerebellar Neurons via Oxidant Stress and Glutathione Depletion.Antioxidants (Basel, Switzerland) · 2022Article
- Effects of Fu's subcutaneous needling on mitochondrial structure and function in rats with sciatica.Molecular pain · 2022Article
- Metabolic Changes in Brain Slices over Time: a Multiplatform Metabolomics Approach.Molecular neurobiology · 2021Article
- NIPSNAP protein family emerges as a sensor of mitochondrial health.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Review
- Improvement of Oxidative Stress and Mitochondrial Dysfunction byAntioxidants (Basel, Switzerland) · 2021Review
- Fine-Tuning the Biological Profile of Multitarget Mitochondriotropic Antioxidants for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Article
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- Biochanin A Attenuates Ovariectomy-Induced Cognition DeficitFrontiers in pharmacology · 2021Article
- Carvacrol andIranian journal of basic medical sciences · 2020Article
- Beneficial Effects of Theta-Burst Transcranial Magnetic Stimulation on Stroke Injury via Improving Neuronal Microenvironment and Mitochondrial Integrity.Translational stroke research · 2020Article
- Whole blood transcriptomic profiles can differentiate vulnerability to chronic low back pain.PloS one · 2019Article
- Ketogenic diet attenuates cerebellar atrophy progression in a subject with a biallelic variant at theThe application of clinical genetics · 2019Article
- Bioconversion of Corticosterone into Corticosterone-Glucoside by Glucosyltransferase.Molecules (Basel, Switzerland) · 2018Article
- The Effect of Associated Parkinsonism on Rehabilitation in Stroke Patients: A Case Series.Sisli Etfal Hastanesi tip bulteni · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Besides fluorine, oxygen is the most electronegative element with the highest reduction potential in biological systems. Metabolic pathways in mammalian cells utilize oxygen as the ultimate oxidizing agent to harvest free energy. They are very efficient, but not without risk of generating various oxygen radicals. These cells have good antioxidative defense mechanisms to neutralize these radicals and prevent oxidative stress. However, increased oxidative stress results in oxidative modifications in lipid, protein, and nucleic acids, leading to mitochondrial dysfunction and cell death. Oxidative stress and mitochondrial dysfunction have been implicated in many neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, and stroke-related brain damage. Research has indicated mitochondria play a central role in cell suicide. An increase in oxidative stress causes mitochondrial dysfunction, leading to more production of reactive oxygen species and eventually mitochondrial membrane permeabilization. Once the mitochondria are destabilized, cells are destined to commit suicide. Therefore, antioxidative agents alone are not sufficient to protect neuronal loss in many neurodegenerative diseases. Combinatorial treatment with antioxidative agents could stabilize mitochondria and may be the most suitable strategy to prevent neuronal loss. This review discusses recent work related to oxidative toxicity in the central nervous system and strategies to treat neurodegenerative diseases.
Identifiers
What OpenQuestion holds
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.