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

Zhong, Xingwu; Yi, Xing; Sá, Rita de Cássia da Silveira e; Zhou, Yujing; Liu, Kaihua; Xiao, Fang; Zhong, Caigao

doi:10.3390/ijms18040816

Cited by 29 publications

(14 citation statements)

References 59 publications

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“…Apoptosis, which is characterized with nuclear fixation, cell shrinkage, DNA fragmentation, and cell membrane bubbles, is a tightly controlled cell death pattern [ 20 , 21 ]. The extrinsic pathway, named the death-receptor pathway, and the intrinsic pathway, named mitochondria-dependent pathway, are the two crucial pathways that are related to apoptosis [ 22 ]. The intrinsic pathway is mediated by Bcl-2 protease family which include apoptotic factors (Bax, Bim, Bak, Noxa, et al) and anti-apoptotic factors (Bcl-2, Mel-1, Bcl-w, et al).…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms of Apoptosis in HepaRG Cell Line Induced by Polyphyllin VI via the Fas Death Pathway and Mitochondrial-Dependent Pathway

Liu

Dong

Wang

et al. 2018

Toxins

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Polyphyllin VI, which is an active saponin, is mainly isolated from traditional medicinal plant Paris polyphylla, which causes liver damage in rats. In the present study, we aimed to explore the potential cytotoxicity of polyphyllin VI on the growth of HepaRG cells and to determine the molecular mechanism. The results revealed that polyphyllin VI changed cell morphology and induced apoptosis in HepaRG cells. Flow cytometric assay displayed that polyphyllin VI promoted the generation of reactive oxygen species (ROS), depolarized the mitochondrial membrane potential (MMP), and induced S phase cell cycle arrest by decreasing the expression of cyclin A2 and CDK2, while significantly increasing the expression of p21 protein. Polyphyllin VI induced the release of cytochrome c from the mitochondria to the cytosol and activated Fas, caspase-3, -8, -9, and PARP proteins. Pretreatment with NAC and Z-VAD-FMK (ROS scavenger and caspase inhibitor, respectively) on HepaRG cells increased the percentage of viable cells, which indicated that polyphyllin VI induced cell apoptosis through mitochondrial pathway by the generation of ROS and Fas death-dependent pathway. All of the effects are in dose- and time-dependent manners. Taken together, these findings emphasize the necessity of risk assessment to polyphyllin VI and offer an insight into polyphyllin VI-induced apoptosis of HepaRG cells.

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Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms of Apoptosis in HepaRG Cell Line Induced by Polyphyllin VI via the Fas Death Pathway and Mitochondrial-Dependent Pathway

Liu

Dong

Wang

et al. 2018

Toxins

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“…Reactive oxygen species (ROS) are engendered in the oxidation-reduction procedure [ 1 ]. ROS, as products of the oxidation and peroxidation process, are instantaneously detoxified by ROS scavengers and antioxidants under physiological conditions [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

“…Ubiquinone (UB), also known as coenzyme Q10 [ 15 , 16 ], is a coenzyme that is regarded as a vitamin-like lipid soluble substance [ 17 , 18 , 19 ]. UB is a vital cofactor in the mitochondrial respiratory chain and plays a fundamental role in oxidative phosphorylation to allow ATP production [ 1 , 20 , 21 ]. Accordingly, UB plays a critical role in energy biosynthesis within the cells and serves as a cofactor in cellular bioenergetics [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…UB deficiency may bring about mitochondrial dysfunction, leading to the generation of ROS. The capability of ROS eliminating is weakened, potentially further aggravating the accumulation of ROS because of UB deficiency [ 1 ]. The fundamental roles of UB include energy biosynthesis and conversion, antioxidant regeneration, antioxidant activity, and its status as a cofactor for enzymatic reactions; accordingly, it has found applications as a drug, nutriment supplement, and cosmetic agent [ 2 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Ubidecarenone-Loaded Nanostructured Lipid Carrier (UB-NLC): Percutaneous Penetration and Protective Effects Against Hydrogen Peroxide-Induced Oxidative Stress on HaCaT Cells

Wang

Xia

2018

IJMS

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The objective of the investigation was to evaluate the percutaneous penetration of a ubidecarenone-loaded nanostructured lipid carrier (UB-NLC) and to illuminate the protective effects of UB-NLC for amelioration of hydrogen peroxide-induced oxidative damage on HaCaT cells. Ubidecarenone (UB) was encapsulated in a nanostructured lipid carrier (NLC), which was manufactured by homogenization. The morphological and dimensional properties of the prepared UB-NLC were studied by freeze-fracture transmission electron microscopy (FF-TEM) and photon correlation spectroscopy (PCS). Percutaneous penetration of UB-NLC was carried out by the Franz diffusion cells method. The change of cellular morphology was identified through a non-invasive time-lapse imaging system. The assessment was achieved via the evaluation of the levels of oxidative stress markers: reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA). Percutaneous penetration of UB loaded in NLC formulation was enhanced in comparison to free UB. Preincubation of HaCaT cells with UB-NLC attenuated the level of intracellular generation of ROS. Lipid peroxidation was diminished by UB-NLC via inhibition of MDA formation. Pretreatment of cells with UB-NLC reestablished the activity of cellular antioxidant enzymes (SOD and GSH-PX). On the basis of the investigation conducted, results suggest that formulating UB as NLC is advantageous for topical delivery and treatment of oxidative stress-induced human diseases.

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“…To investigate the toxic mechanism of hexavalent chromium Cr(VI) and to 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 by Zhong et al [ 12 ]. They found that the gene expression of electron transfer flavoprotein dehydrogenase (ETFDH) was strongly downregulated by Cr(VI) exposure.…”

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confidence: 99%