Mitochondrial respiratory chain dysfunction mediated by ROS is a primary point of fluoride-induced damage in Hepa1-6 cells

Wang, Hongwei; Zhang, Yan; Tan, Panpan; Jia, Liu-shu; Chen, Yu

doi:10.1016/j.envpol.2019.113359

Cited by 39 publications

(17 citation statements)

References 58 publications

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“…The yield of ROS produced by the ETC increase during hypoxia, light stimulation, ischemia-reperfusion, aging, and mitochondrial respiratory depression. Over 90% of the oxygen in mitochondria is reduced by cytochrome oxidase to water molecules, while only 0.1%-0.2% of O 2 forms ROS through electron flow, mainly through electron transport chain complexes I and III[ 15 , 36 ]. The rate of the ROS produced by mitochondria is mainly affected by mitochondrial membrane potential (MMP) regulation.…”

Section: Production and Metabolism Of Ros During Pdtmentioning

confidence: 99%

“…Therefore, the main target position of the photochemical reaction in the cell is often near the subcellular components where the PS is localized, which explains the heterogeneity of the effects of different PSs[ 14 ]. On the other hand, the metabolic induction of mitochondrial ROS production is much more complicated; for example, it may involve the partial inactivation of respiratory complexes I, II, and III of the mitochondrial electron transport chain[ 15 ]. In general, excessive ROS destroy the redox system in cells and cause oxidative damage to biomolecules, including DNA and other molecules[ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Zhang

Wang

et al. 2020

WJSC

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Photodynamic therapy (PDT) is an effective and promising cancer treatment. PDT directly generates reactive oxygen species (ROS) through photochemical reactions. This oxygen-dependent exogenous ROS has anti-cancer stem cell (CSC) effect. In addition, PDT may also increase ROS production by altering metabolism, endoplasmic reticulum stress, or potential of mitochondrial membrane. It is known that the half-life of ROS in PDT is short, with high reactivity and limited diffusion distance. Therefore, the main targeting position of PDT is often the subcellular localization of photosensitizers, which is helpful for us to explain how PDT affects CSC characteristics, including differentiation, self-renewal, apoptosis, autophagy, and immunogenicity. Broadly speaking, excess ROS will damage the redox system and cause oxidative damage to molecules such as DNA, change mitochondrial permeability, activate unfolded protein response, autophagy, and CSC resting state. Therefore, understanding the molecular mechanism by which ROS affect CSCs is beneficial to improve the efficiency of PDT and prevent tumor recurrence and metastasis. In this article, we review the effects of two types of photochemical reactions on PDT, the metabolic processes, and the biological effects of ROS in different subcellular locations on CSCs.

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Section: Production and Metabolism Of Ros During Pdtmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Zhang

Wang

et al. 2020

WJSC

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“…Mitochondria, as the main oxidative energy producers in eukaryotic cells, consist of five protein complexes, including NADH dehydrogenase (Complex I), succinate dehydrogenase (Complex II), ubiquinol cytochrome c oxidoreductase (Complex III), cytochrome c oxidase (Complex IV), and ATP synthase (Complex V). Dysregulated protein levels of any of these complexes can be indicative of mitochondrial disorder ( 4 ). Furthermore, mitochondrial autophagy, a conserved self-digestion process, plays a key role in the maintenance of cell homeostasis, and dysregulation of autophagy often occurs during tumor development ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy

Xie

Zhang

et al. 2020

Front. Oncol.

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Esophageal squamous cell carcinoma (ESCC) has a worldwide impact on human health, due to its high incidence and mortality. Therefore, identifying compounds to increase patients' survival rate is urgently needed. Mefloquine (MQ) is an FDA-approved anti-malarial drug, which has been reported to inhibit cellular proliferation in several cancers. However, the anti-tumor activities of the drug have not yet been completely defined. In this study, mass spectrometry was employed to profile proteome changes in ESCC cells after MQ treatment. Sub-cellular localization and gene ontology term enrichment analysis suggested that MQ treatment mainly affect mitochondria. The KEGG pathway enrichment map of down-regulated pathways and Venn diagram indicated that all of the top five down regulated signaling pathways contain four key mitochondrial proteins (succinate dehydrogenase complex subunit C (SDHC), succinate dehydrogenase complex subunit D, mitochondrially encoded cytochrome c oxidase III and NADH: ubiquinone oxidoreductase subunit V3). Meanwhile, mitochondrial autophagy was observed in MQ-treated KYSE150 cells. More importantly, patient-derived xenograft mouse models of ESCC with SDHC high expression were more sensitive to MQ treatment than low SDHC-expressing xenografts. Taken together, mefloquine inhibits ESCC tumor growth by inducing mitochondrial autophagy and SDHC plays a vital role in MQ-induced anti-tumor effect on ESCC.

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“…34 ROS are byproducts of aerobic metabolism, which induces mutilation to lipids, proteins and DNA, and oxidative stress refers to high intracellular expression of ROS. 35,36 Adenovirus-mediated upregulation of MsrA can significantly regress hypoxia-induced elevation in ROS levels and foster cell survival, thereby exhibiting the protective properties of MsrA against hypoxia/reoxygenation-induced cell injury and suggesting its therapeutic potential in ischemic heart and brain diseases. 37 The function of SOD has been identified in many inflammatory diseases, neurodegenerative diseases as well as ischemia and reperfusion diseases.…”

Section: Discussionmentioning

confidence: 99%

<p>MsrA Suppresses Inflammatory Activation of Microglia and Oxidative Stress to Prevent Demyelination via Inhibition of the NOX2-MAPKs/NF-κB Signaling Pathway</p>

Fan¹,

Li²,

Guan

et al. 2020

DDDT

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Introduction: Demyelination causes neurological deficits involving visual, motor, sensory symptoms. Deregulation of several enzymes has been identified in demyelination, which holds potential for the development of treatment strategies for demyelination. However, the specific effect of methionine sulfoxide reductase A (MsrA) on demyelination remains unclear. Hence, this study aims to explore the effect of MsrA on oxidative stress and inflammatory response of microglia in demyelination. Methods: Initially, we established a mouse model with demyelination induced by cuprizone and a cell model provoked by lipopolysaccharide (LPS). The expression of MsrA in wildtype (WT) and MsrA-knockout (MsrA-/-) mice were determined by RT-qPCR and Western blot analysis. In order to further explore the function of MsrA on inflammatory response, and oxidative stress in demyelination, we detected the expression of microglia marker Iba1, inflammatory factors TNF-α and IL-1β and intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) activity, as well as expression of the NOX2-MAPKs/NF-κB signaling pathway-related genes in MsrA-/mice and LPS-induced microglia following different treatments. Results: MsrA expression was downregulated in MsrA-/mice. MsrA silencing was shown to produce severely injured motor coordination, increased expressions of Iba1, TNF-α, IL-1β, ROS and NOX2, and extent of ERK, p38, IκBα, and p65 phosphorylation, but reduced SOD activity. Conjointly, our study suggests that Tat-MsrA fusion protein can prevent the cellular inflammatory response and subsequent demyelination through negative regulation of the NOX2-MAPKs/NF-κB signaling pathway. Conclusion: Our data provide a profound insight on the role of endogenous antioxidative defense systems such as MsrA in controlling microglial function.

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Mitochondrial respiratory chain dysfunction mediated by ROS is a primary point of fluoride-induced damage in Hepa1-6 cells

Cited by 39 publications

References 58 publications

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Photodynamic therapy regulates fate of cancer stem cells through reactive oxygen species

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy

<p>MsrA Suppresses Inflammatory Activation of Microglia and Oxidative Stress to Prevent Demyelination via Inhibition of the NOX2-MAPKs/NF-κB Signaling Pathway</p>

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