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- Title
CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.
- Authors
Xiali Zhong; Xing Yi; da Silveira e Sá, Rita de Cássia; Yujing Zhang; Kaihua Liu; Fang Xiao; Caigao Zhong
- Abstract
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 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.
- Subjects
HEXAVALENT chromium; DICARBOXYLIC acids; GENE expression; BAX protein; BCL-2 proteins
- Publication
International Journal of Molecular Sciences, 2017, Vol 18, Issue 4, p816
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms18040816