<i>Portulaca oleracea</i> Linn seed extract ameliorates hydrogen peroxide-induced cell death in human liver cells by inhibiting reactive oxygen species generation and oxidative stress

Reactive oxygen species (ROS) are highly reactive reduced oxygen molecules that result from aerobic metabolism. The common forms are the superoxide anion (O2∙−) and hydrogen peroxide (H2O2) and their derived forms, hydroxyl radical (HO∙) and hydroperoxyl radical (HOO∙). Their production sites in mitochondria are reviewed. Even though being highly toxic products, ROS seem important in transducing information from dysfunctional mitochondria. Evidences of signal transduction mediated by ROS in mitochondrial deficiency contexts are then presented in different organisms such as yeast, mammals or photosynthetic organisms.

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Early joint degeneration and antagonism between growth factors and reactive oxygen species. Is non-surgical management possible?

Joints ◽

10.11138/jts/2015.3.3.123 ◽

2015 ◽

Vol 03 (03) ◽

pp. 123-128 ◽

Cited By ~ 3

Author(s):

Andrea Manunta ◽

Pietro Zedde ◽

Sebastiano Cudoni ◽

Gianfilippo Caggiari ◽

Gianfranco Pintus

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Hydrogen Peroxide ◽

Cell Death ◽

Growth Factors ◽

Protective Effect ◽

Blood Serum ◽

Reactive Oxygen ◽

Oxygen Species ◽

Serum Samples

Purpose: in pathological conditions such as osteoarthritis (OA), overproduction of reactive oxygen species (ROS) may overwhelm the antioxidant defenses of chondrocytes, thus promoting oxidative stress and cell death. It can be hypothesized that increasing the antioxidant machinery of chondrocytes may prevent the age-associated progression of this disease. Growth factors (GFs) play an important role in promoting both the resolution of inflammatory processes and tissue repair. in view of these considerations, we set out to investigate the protective effect, against H2O2-induced oxidative cell death, potentially exerted by fluid drained from the joint postoperatively. Methods: the present study was conducted in 20 patients diagnosed with bilateral knee osteoarthritis and treated, between January 2013 and June 2014, with prosthetic knee implantation on the side more affected by the arthritic process, together with intraoperative placement of a closed-circuit drainage aspiration system. As a result, 20 different serum samples were collected from the drained articular fluid, prepared using two different methodologies. In addition, forty blood serum samples were obtained and prepared: 20 from the surgically treated patients and 20 from healthy controls. The present work was undertaken to investigate the potential protective effect of sera obtained from articular fluid drainage against hydrogen peroxide-induced oxidative stress in cultured human chondrocytes. Results: exposure of chondrocytes to hydrogen peroxide elicited a dose-dependent increase in oxidative stress and chondrocyte cell death, phenomena that were significantly counteracted by the pre-treatment of cell cultures with sera from articular fluid drainage. Conclusions: oxidatively stressed chondrocytes treated with sera obtained from articular fluid drainage lived longer than those treated with blood serum samples and longer than untreated ones. Clinical Relevance: synovial fluids are usually discarded once the drainage reservoir is full; instead they could benefit the patients from whom they are collected, as they are rich in growth factors and they may act as antagonists of ROS effects. Accordingly, they could be used to treat chondropathies, early OA, and mild OA located in other sites.

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Heat-shock-induced oxidative stress and antioxidant response in Aspergillus niger 26

Canadian Journal of Microbiology ◽

10.1139/w08-091 ◽

2008 ◽

Vol 54 (12) ◽

pp. 977-983 ◽

Cited By ~ 48

Author(s):

Radoslav I. Abrashev ◽

Svetlana B. Pashova ◽

Lilyana N. Stefanova ◽

Spassen V. Vassilev ◽

Pavlina A. Dolashka-Angelova ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Heat Shock ◽

Aspergillus Niger ◽

Reactive Oxygen Species Generation ◽

Reactive Oxygen ◽

Antioxidant Response ◽

Temperature Treatment ◽

Oxygen Species ◽

And Oxidative Stress

To extend the knowledge about the relationship between heat shock and oxidative stress in lower eukaryotes, the filamentous fungus Aspergillus niger 26 was chosen as a model system. Here, the response of A. niger cells to heat shock is reported. The temperature treatment significantly increased the levels of reactive oxygen species, superoxide anions (O2•–), and hydrogen peroxide and the rate of cyanide-resistant respiration as a marker of oxidative stress. Enhanced reactive oxygen species generation coincided with an increase in the content of oxidative damaged protein and in the accumulation of the storage carbohydrates trehalose and glycogen. Thermal survival of the A. niger cells corresponded to a significant increase in the levels of the antioxidant enzymes superoxide dismutase and catalase for all variants. These observations suggest that heat and oxidative stress have a common cellular effect.

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4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/1670759 ◽

2019 ◽

Vol 2019 ◽

pp. 1-16 ◽

Cited By ~ 2

Author(s):

Amnah M. Alshangiti ◽

Eszter Tuboly ◽

Shane V. Hegarty ◽

Cathal M. McCarthy ◽

Aideen M. Sullivan ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Cell Death ◽

Cytotoxic Effect ◽

Neuroblastoma Cells ◽

Reactive Oxygen ◽

Prognostic Indicator ◽

Oxygen Species ◽

Human Neuroblastoma Cells ◽

Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

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Intracellular Sources of ROS/H2O2 in Health and Neurodegeneration: Spotlight on Endoplasmic Reticulum

Cells ◽

10.3390/cells10020233 ◽

2021 ◽

Vol 10 (2) ◽

pp. 233

Author(s):

Tasuku Konno ◽

Eduardo Pinho Melo ◽

Joseph E. Chambers ◽

Edward Avezov

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Hydrogen Peroxide ◽

Endoplasmic Reticulum ◽

Neurodegenerative Diseases ◽

Antioxidative Enzymes ◽

Redox Reactions ◽

Ros Production ◽

Oxygen Species ◽

Specific Target

Reactive oxygen species (ROS) are produced continuously throughout the cell as products of various redox reactions. Yet these products function as important signal messengers, acting through oxidation of specific target factors. Whilst excess ROS production has the potential to induce oxidative stress, physiological roles of ROS are supported by a spatiotemporal equilibrium between ROS producers and scavengers such as antioxidative enzymes. In the endoplasmic reticulum (ER), hydrogen peroxide (H2O2), a non-radical ROS, is produced through the process of oxidative folding. Utilisation and dysregulation of H2O2, in particular that generated in the ER, affects not only cellular homeostasis but also the longevity of organisms. ROS dysregulation has been implicated in various pathologies including dementia and other neurodegenerative diseases, sanctioning a field of research that strives to better understand cell-intrinsic ROS production. Here we review the organelle-specific ROS-generating and consuming pathways, providing evidence that the ER is a major contributing source of potentially pathologic ROS.

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Momordica charantia L. Induces Non-Apoptotic Cell Death in Human MDA-MB-436 Breast and A549 Lung Cancer Cells by Disrupting Energy Metabolism and Exacerbating Reactive Oxygen Species’ Generation

Journal of Ethnopharmacology ◽

10.1016/j.jep.2021.114036 ◽

2021 ◽

pp. 114036

Author(s):

Adeola Folasade Ehigie ◽

Peng Wei ◽

Taotao Wei ◽

Xiyun Yan ◽

Olufunso O. Olorunsogo ◽

...

Keyword(s):

Lung Cancer ◽

Reactive Oxygen Species ◽

Cell Death ◽

Energy Metabolism ◽

Cancer Cells ◽

Apoptotic Cell ◽

Reactive Oxygen Species Generation ◽

Lung Cancer Cells ◽

Oxygen Species ◽

A549 Lung

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Toxicity assessment of metallic nickel nanoparticles in various biological models: An interplay of reactive oxygen species, oxidative stress, and apoptosis

Toxicology and Industrial Health ◽

10.1177/07482337211011008 ◽

2021 ◽

pp. 074823372110110

Author(s):

Shabnoor Iqbal ◽

Farhat Jabeen ◽

Abdul Shakoor Chaudhry ◽

Muhammad Ajmal Shah ◽

Gaber El-Saber Batiha

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Nickel Nanoparticles ◽

Hypoxia Inducible Factor ◽

Reactive Oxygen Species Generation ◽

Reactive Oxygen ◽

Volume Ratio ◽

Nuclear Factor Κb ◽

Metallic Nickel ◽

Oxygen Species

Nickel nanoparticles (Ni-NPs) are widely used for multiple purposes in industries. Ni-NPs exposure is detrimental to ecosystems owing to widespread use, and so their toxicity is important to consider for real-world applications. This review mainly focuses on the notable pathophysiological activities of Ni-NPs in various research models. Ni-NPs are stated to be more toxic than bulk forms because of their larger surface area to volume ratio and are reported to provoke toxicity through reactive oxygen species generation, which leads to the upregulation of nuclear factor-κB and promotes further signaling cascades. Ni-NPs may contribute to provoking oxidative stress and apoptosis. Hypoxia-inducible factor 1α and mitogen-activated protein kinases pathways are involved in Ni-NPs associated toxicity. Ni-NPs trigger the transcription factors p-p38, p-JNK, p-ERK1/2, interleukin (IL)-3, TNF-α, IL-13, Fas, Cyt c, Bax, Bid protein, caspase-3, caspase-8, and caspase-9. Moreover, Ni-NPs have an occupational vulnerability and were reported to induce lung-related disorders owing to inhalation. Ni-NPs may cause serious effects on reproduction as Ni-NPs induced deleterious effects on reproductive cells (sperm and eggs) in animal models and provoked hormonal alteration. However, recent studies have provided limited knowledge regarding the important checkpoints of signaling pathways and less focused on the toxic limitation of Ni-NPs in humans, which therefore needs to be further investigated.

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Novel Antioxidant Properties of Doxycycline

International Journal of Molecular Sciences ◽

10.3390/ijms19124078 ◽

2018 ◽

Vol 19 (12) ◽

pp. 4078 ◽

Cited By ~ 9

Author(s):

Dahn Clemens ◽

Michael Duryee ◽

Cleofes Sarmiento ◽

Andrew Chiou ◽

Jacob McGowan ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Hydrogen Peroxide ◽

Chronic Inflammation ◽

Antioxidant Properties ◽

Antibacterial Properties ◽

Reactive Oxygen ◽

Protein Adducts ◽

Oxygen Species ◽

Free System

Doxycycline (DOX), a derivative of tetracycline, is a broad-spectrum antibiotic that exhibits a number of therapeutic activities in addition to its antibacterial properties. For example, DOX has been used in the management of a number of diseases characterized by chronic inflammation. One potential mechanism by which DOX inhibits the progression of these diseases is by reducing oxidative stress, thereby inhibiting subsequent lipid peroxidation and inflammatory responses. Herein, we tested the hypothesis that DOX directly scavenges reactive oxygen species (ROS) and inhibits the formation of redox-mediated malondialdehyde-acetaldehyde (MAA) protein adducts. Using a cell-free system, we demonstrated that DOX scavenged reactive oxygen species (ROS) produced during the formation of MAA-adducts and inhibits the formation of MAA-protein adducts. To determine whether DOX scavenges specific ROS, we examined the ability of DOX to directly scavenge superoxide and hydrogen peroxide. Using electron paramagnetic resonance (EPR) spectroscopy, we found that DOX directly scavenged superoxide, but not hydrogen peroxide. Additionally, we found that DOX inhibits MAA-induced activation of Nrf2, a redox-sensitive transcription factor. Together, these findings demonstrate the under-recognized direct antioxidant property of DOX that may help to explain its therapeutic potential in the treatment of conditions characterized by chronic inflammation and increased oxidative stress.

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