ArticleInternational journal of molecular sciences2017
CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Coenzyme Q10 Attenuates Kidney Injury Induced by Titanium Dioxide Nanoparticles and Cadmium Co-exposure in Rats.Biological trace element research · 2025Article
- Activating PPARβ/δ-Mediated Fatty Acid β-Oxidation Mitigates Mitochondrial Dysfunction Co-induced by Environmentally Relevant Levels of Molybdenum and Cadmium in Duck Kidneys.Biological trace element research · 2025Article
- Chitosan attenuates titanium dioxide nanoparticles induced hepatic and renal toxicities.Scientific reports · 2025Article
- Increased risk of rhabdomyolysis in patients using statins: a population-based case-control study.Therapeutic advances in drug safety · 2025Article
- Research progress of mitochondrial dysfunction induced pyroptosis in acute lung injury.Respiratory research · 2024Review
- The Scavenging Activity of Coenzyme QInternational journal of molecular sciences · 2024Article
- Article
- Adaptive responses to neurodegenerative stress in glaucoma.Progress in retinal and eye research · 2021Review
- Coenzyme QBMC pharmacology & toxicology · 2021Article
- Effects of Cr(VI) exposure on electrocardiogram, myocardial enzyme parameters, inflammatory factors, oxidative kinase, and ATPase of the heart in Chinese rural dogs.Environmental science and pollution research international · 2019Article
- Hepatic and Renal Toxicity Induced by TiOJournal of toxicology · 2019Article
- Ubidecarenone-Loaded Nanostructured Lipid Carrier (UB-NLC): Percutaneous Penetration and Protective Effects Against Hydrogen Peroxide-Induced Oxidative Stress on HaCaT Cells.International journal of molecular sciences · 2018Article
- Chemically-Induced DNA Damage, Mutagenesis, and Cancer.International journal of molecular sciences · 2018Article
- Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the toxic mechanism of hexavalent chromium Cr(VI) and search for an antidote for Cr(VI)-induced cytotoxicity, a study of mitochondrial dysfunction induced by Cr(VI) and cell survival by recovering mitochondrial function was performed. In the present study, we found that the gene expression of electron transfer flavoprotein dehydrogenase (ETFDH) was strongly downregulated by Cr(VI) exposure. The levels of coenzyme 10 (CoQ10) and mitochondrial biogenesis presented by mitochondrial mass and mitochondrial DNA copy number were also significantly reduced after Cr(VI) exposure. The subsequent, Cr(VI)-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species (ROS) accumulation, caspase-3 and caspase-9 activation, decreased superoxide dismutase (SOD) and ATP production, increased methane dicarboxylic aldehyde (MDA) content, mitochondrial membrane depolarization and mitochondrial permeability transition pore (MPTP) opening, increased Ca
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