Next Article in Journal
Role of RHEB in Regulating Differentiation Fate of Mesenchymal Stem Cells for Cartilage and Bone Regeneration
Next Article in Special Issue
Significance of Wild-Type p53 Signaling in Suppressing Apoptosis in Response to Chemical Genotoxic Agents: Impact on Chemotherapy Outcome
Previous Article in Journal
Commitment of Scaffold Proteins in the Onco-Biology of Human Colorectal Cancer and Liver Metastases after Oxaliplatin-Based Chemotherapy
Previous Article in Special Issue
Supercritical-Carbon Dioxide Fluid Extract from Chrysanthemum indicum Enhances Anti-Tumor Effect and Reduces Toxicity of Bleomycin in Tumor-Bearing Mice
Open AccessArticle

CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity

Department of Health Toxicology, School of Public Health, Central South University, Changsha 410008, China
Department of Environmental Health Science, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA
Department of Physiology and Pathology, Health Sciences Center, Federal University of Paraíba, 58059-900 João Pessoa, Brazil
Author to whom correspondence should be addressed.
Academic Editors: Ashis Basu and Takehiko Nohmi
Int. J. Mol. Sci. 2017, 18(4), 816;
Received: 11 February 2017 / Revised: 3 April 2017 / Accepted: 7 April 2017 / Published: 24 April 2017
(This article belongs to the Special Issue Chemically-Induced DNA Damage, Mutagenesis, and Cancer)
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 Ca2+ levels, Cyt c release, decreased Bcl-2 expression, and significantly elevated Bax expression. The Cr(VI)-induced deleterious changes were attenuated by pretreatment with CoQ10 in L-02 hepatocytes. These data suggest that Cr(VI) induces CoQ10 deficiency in L-02 hepatocytes, indicating that this deficiency may be a biomarker of mitochondrial dysfunction in Cr(VI) poisoning and that exogenous administration of CoQ10 may restore mitochondrial function and protect the liver from Cr(VI) exposure. View Full-Text
Keywords: hexavalent chromium Cr(VI); coenzyme Q10; reactive oxygen species (ROS); mitochondrial membrane potential (MMP); L-02 hepatocytes; apoptosis hexavalent chromium Cr(VI); coenzyme Q10; reactive oxygen species (ROS); mitochondrial membrane potential (MMP); L-02 hepatocytes; apoptosis
Show Figures

Graphical abstract

MDPI and ACS Style

Zhong, X.; Yi, X.; Da Silveira e Sá, R.D.C.; Zhang, Y.; Liu, K.; Xiao, F.; Zhong, C. CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity. Int. J. Mol. Sci. 2017, 18, 816.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

Back to TopTop