ArticleTheScientificWorldJournal2012
Mitochondrial electron transport chain in heavy metal-induced neurotoxicity: effects of cadmium, mercury, and copper.
Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
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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
59 citing papers in PubMed, 168 citations in OpenAlex.
- Pollutant Exposure Shapes Mitochondrial Bioenergetics in a Wild Seabird.Environment & health (Washington, D.C.) · 2026Article
- Understanding molecular mechanisms driving cadmium-induced mitochondrial dysfunction in human metabolic liver disease.Environmental toxicology and pharmacology · 2026Review
- Unveiling the Metabolic Fingerprint of Occupational Exposure in Ceramic Manufactory Workers.Toxics · 2026Article
- Developmental and lifelong exposure to mercury chloride exacerbates cognitive and motor decline in aged mice.AIMS neuroscience · 2026Article
- SIRT1 regulates dermal fibroblast senescence via impaired deacetylase function and mitochondrial dysfunction during skin aging induced by chronic oral cadmium exposure.Frontiers in public health · 2026Article
- Characterization of Metabolomic Response ofMicroorganisms · 2025Article
- Application of Modulators of CaInternational journal of molecular sciences · 2025Article
- The molecular mechanisms of cuproptosis and its relevance to atherosclerosis.Biomolecules & biomedicine · 2025Review
- Article
- Copper's new role in cancer: how cuproptosis-related genes could revolutionize glioma treatment.BMC cancer · 2025Article
- Membrane transporters modulating the toxicity of arsenic, cadmium, and mercury in human cells.Life science alliance · 2025Article
- Heavy Metal Exposure: Molecular Pathways, Clinical Implications, and Protective Strategies.Antioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial pathways of copper neurotoxicity: focus on mitochondrial dynamics and mitophagy.Frontiers in molecular neuroscience · 2024Review
- Review
- Increased cytotoxicity of PbEnvironmental science. Processes & impacts · 2023Article
- Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria.International journal of molecular sciences · 2023Review
- Mitochondria in the Spotlight:Cells · 2023Review
- Copper metabolism in cell death and autophagy.Autophagy · 2023Review
- The genetic basis of adaptation to copper pollution inFrontiers in genetics · 2023Article
- Ferulic Acid Activates SIRT1-Mediated Ferroptosis Signaling Pathway to Improve Cognition Dysfunction in Wilson's Disease.Neuropsychiatric disease and treatment · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To clarify the role of mitochondrial electron transport chain (mtETC) in heavy-metal-induced neurotoxicity, we studied action of Cd(2+), Hg(2+), and Cu(2+) on cell viability, intracellular reactive oxygen species formation, respiratory function, and mitochondrial membrane potential of rat cell line PC12. As found, the metals produced, although in a different way, dose- and time-dependent changes of all these parameters. Importantly, Cd(2+) beginning from 10 [mu]M and already at short incubation time (3 h) significantly inhibited the FCCP-uncoupled cell respiration; besides, practically the complete inhibition of the respiration was reached after 3 h incubation with 50 [mu]M Hg(2+) or 500 [mu]M Cd(2+), whereas even after 48 h exposure with 500 [mu]M Cu(2+), only a 50% inhibition of the respiration occurred. Against the Cd(2+)-induced cell injury, not only different antioxidants and mitochondrial permeability transition pore inhibitors were protective but also such mtETC effectors as FCCP and stigmatellin (complex III inhibitor). However, all mtETC effectors used did not protect against the Hg(2+)- or Cu(2+)-induced cell damage. Notably, stigmatellin was shown to be one of the strongest protectors against the Cd(2+)-induced cell damage, producing a 15-20% increase in the cell viability. The mechanisms of the mtETC involvement in the heavy-metal-induced mitochondrial membrane permeabilization and cell death are discussed.
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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.