Mitochondrial Free Radicals, Antioxidants, Nutrient Substances, and Chronic Hepatitis C

Guo, Chih-Hung; Chen, Pei-Chung

doi:10.5772/51315

Cited by 5 publications

(5 citation statements)

References 183 publications

(178 reference statements)

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“…The comparatively high level of ROS would be excessive for chondrocytes that normally reside in a physiologically hypoxic condition, and causes damages, especially to mitochondrial function [24,25], resulting in reduction of DNA integrity and damage repair and leading to cell death [45,46]. The mitochondria are a "power station" of the cell, participate in the process of signal transduction and in cellular activities, including sensing the redox homeostasis [20] and producing non-enzymatic and enzymatic antioxidants, but mitochondria are generally devoid of CAT [47] for defending from oxidative stress. In fact, the 3 dosages of CAT provided enough activity in this study capable of scavenging systematic ROS by bringing the intracellular H 2 O 2 to a significant low level of < 1/3 of that in untreated control cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Catalase Enhances Viability of Human Chondrocytes in Culture by Reducing Reactive Oxygen Species and Counteracting Tumor Necrosis Factor-α-Induced Apoptosis

Yang

Feng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Both physiologic remodeling and pathologic regeneration of cartilage tissue rely upon chondrocyte functions and are benefited from factors that promote viability and inhibit apoptosis of the cell, and associated mechanisms. High level of reactive oxygen species (ROS) and proinflammatory cytokines activate apoptosis signaling and initiate cell death, which can be attenuated by antioxidants. This study examined the effect of catalase (CAT) on ROS and tumor necrosis factor-α (TNF-α)-induced apoptosis in human C28/I2 chondrocytes cultured in monolayer. Methods: Chondrocytes were treated with diluted CAT in the presence or absence of TNF-α and compared to untreated cells. Levels of hydrogen peroxide (H₂O₂) and mitochondrial membrane potential (Δψ_m) were measured using fluorescent labeling, cell apoptosis was assayed by flow cytometry using Annexin V/propidium iodide (PI) staining, gene expression was detected by quantitative real time polymerase chain reaction (qRT-PCR) and the proteins were investigated by Western blotting. Results: CAT effectively reduced the intracellular ROS caused by the monolayer culture system, enhanced the Δψ_m depending on the presence of TNF-α and promoted morphological features at sub-cellular level. CAT also attenuated the TNF-α-upregulated expression of factors/mediators of extrinsic cell death cascade and apoptotic caspases, ultimately resulted in promoted cellular viability. Conclusion: The anti-apoptotic effect of CAT on chondrocytes via scavenging ROS and suppressing TNF-α-induced cell apoptosis by TNF/TNF receptor (TNFR) mediated death signaling pathway and potentiate CAT as a complementary agent beneficial to cartilage remodeling and regeneration in vivo, and cell-based therapies of cartilage repair demanding viable cells expanded ex vivo.

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Section: Discussionmentioning

confidence: 99%

Catalase Enhances Viability of Human Chondrocytes in Culture by Reducing Reactive Oxygen Species and Counteracting Tumor Necrosis Factor-α-Induced Apoptosis

Yang

Feng

et al. 2018

Cell Physiol Biochem

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“…Oxidative stress, defined as a disruption between pro-oxidant and antioxidant systems, can result in cellular damage [31]. Increased oxidative stress in breast tumor tissues compared to the levels in non-malignant tissues has been observed [32,33].…”

Section: Discussionmentioning

confidence: 99%

Distribution of Selenium and Oxidative Stress in Breast Tumor-Bearing Mice

2013

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The present study investigated the effects of breast tumors on the blood and tissue distribution of essential trace mineral selenium (Se), and oxidative stress status of mice. Female 10-week-old BALB/cByJNarl mice were randomly assigned into control (CNL) and breast tumor-bearing (TB) groups. TB mice were injected subcutaneously into the right hind thigh with 5 × 106 EMT6 mouse mammary tumor cells. After 22 days, we measured Se concentrations, Se-dependent glutathione peroxidase (GPx) activities, and malondialdehyde (MDA) products (indicator of oxidative stress) in plasma, various tissues, and plasma vascular endothelial growth factor (VEGF) concentrations. There were no significant differences in body weights and daily intake between both groups. Compared with the CNL group, TB mice have decreases in plasma Se concentrations and GPx activities, as well as higher plasma VEGF and MDA concentrations. Plasma Se concentrations were also negatively correlated with plasma MDA and VEGF concentrations. Furthermore, tissue Se concentrations and GPx activities in TB animals were lower; whereas the MDA concentrations higher in various tissues including liver, kidney, brain, lung, spleen, and thymic tissues. In conclusion, disruption of Se homeostasis critically reflects oxidative stress in target tissues, thus may increase the risk for progression of breast cancer and metastasis.

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“…This is achieved by activating the mitostress signals, via producing ROS and decreasing the inner mitochondrial membrane potential [33]. Also, mitochondria maintain cellular homeostasis by reducing ROS and H 2 O 2 using antioxidant mechanisms, such as manganesedependent superoxide dismutase and glutathione peroxidase [30,55]. Importantly, mitochondria orchestrate the adaptive immunity of the cells by releasing mitochondrial antiviral signaling protein (MAVS), damage-associated molecular pattern protein (DAMP), and mitochondrial ROS [14,48].…”

Section: Function Of the Mitochondria In Normal Cellsmentioning

confidence: 99%

Regulation of mitochondrial temperature in health and disease

El-Gammal

Nasr

Elmehrath

et al. 2022

Pflugers Arch - Eur J Physiol

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Mitochondrial temperature is produced by various metabolic processes inside the mitochondria, particularly oxidative phosphorylation. It was recently reported that mitochondria could normally operate at high temperatures that can reach 50℃. The aim of this review is to identify mitochondrial temperature differences between normal cells and cancer cells. Herein, we discussed the different types of mitochondrial thermosensors and their advantages and disadvantages. We reviewed the studies assessing the mitochondrial temperature in cancer cells and normal cells. We shed the light on the factors involved in maintaining the mitochondrial temperature of normal cells compared to cancer cells.

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Mitochondrial Free Radicals, Antioxidants, Nutrient Substances, and Chronic Hepatitis C

Cited by 5 publications

References 183 publications

Catalase Enhances Viability of Human Chondrocytes in Culture by Reducing Reactive Oxygen Species and Counteracting Tumor Necrosis Factor-α-Induced Apoptosis

Catalase Enhances Viability of Human Chondrocytes in Culture by Reducing Reactive Oxygen Species and Counteracting Tumor Necrosis Factor-α-Induced Apoptosis

Distribution of Selenium and Oxidative Stress in Breast Tumor-Bearing Mice

Regulation of mitochondrial temperature in health and disease

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