scholarly journals The Na/K-ATPase Signaling: From Specific Ligands to General Reactive Oxygen Species

2018 ◽  
Vol 19 (9) ◽  
pp. 2600 ◽  
Author(s):  
Rebecca Pratt ◽  
Cameron Brickman ◽  
Cameron Cottrill ◽  
Joseph Shapiro ◽  
Jiang Liu
Keyword(s):  
Reactive Oxygen Species ◽  
Positive Feedback ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Short Review ◽  
Oxygen Species ◽  
Signaling Function ◽  
Amplification Loop

The signaling function of the Na/K-ATPase has been established for 20 years and is widely accepted in the field, with many excellent reports and reviews not cited here. Even though there is debate about the underlying mechanism, the signaling function is unquestioned. This short review looks back at the evolution of Na/K-ATPase signaling, from stimulation by cardiotonic steroids (also known as digitalis-like substances) as specific ligands to stimulation by reactive oxygen species (ROS) in general. The interplay of cardiotonic steroids and ROS in Na/K-ATPase signaling forms a positive-feedback oxidant amplification loop that has been implicated in some pathophysiological conditions.

scholarly journals Drosophila hemocytes recognize lymph gland tumors of mxc mutants and activate the Toll pathway in reactive oxygen species-dependent manner

2021 ◽  
Author(s):  
Suzuko Kinoshita ◽  
Kazuki Takarada ◽  
Yoshihiro H. Inoue
Keyword(s):  
Reactive Oxygen Species ◽  
Fat Body ◽  
Ectopic Expression ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Matrix Metalloproteinase 1 ◽  
Membrane Components

Mechanisms of cancer cell recognition and elimination by the innate immune system remains unclear. Circulating hemocytes are associated with the hematopoietic tumors in Drosophila mxcmbn1 mutant larvae. The innate immune signalling pathways are activated in the fat body to suppress the tumor growth by inducing antimicrobial peptides (AMP). Here, we investigated the regulatory mechanism underlying the activation in the mutant. Reactive oxygen species accumulated in the hemocytes due to induction of dual oxidase and its activator. The hemocytes were also localized on the fat body. These were essential for transmitting the information on tumors toward the fat body to induce AMP expression. Regarding to the tumor recognition, we found that matrix metalloproteinase 1 (MMP1) and MMP2 were highly expressed in the tumors. Ectopic expression of MMP2 was associated with AMP induction in the mutants. Furthermore, the basement membrane components in the tumors were reduced and ultimately lost. The hemocytes may recognize the disassembly in the tumors. Our findings highlight the underlying mechanism via which macrophage-like hemocytes recognize tumor cells and relay the information toward the fat body to induce AMPs. and contribute to uncover the immune system's roles against cancer.

scholarly journals Selective Activation of Endoplasmic Reticulum Stress by Reactive-Oxygen-Species-Mediated Ochratoxin A-Induced Apoptosis in Tubular Epithelial Cells

2021 ◽  
Vol 22 (20) ◽  
pp. 10951
Author(s):  
Chong-Sun Khoi ◽  
Yu-Wen Lin ◽  
Jia-Huang Chen ◽  
Biing-Hui Liu ◽  
Tzu-Yu Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Ochratoxin A ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Oxygen Species ◽  
Food And Feed ◽  
Renal Proximal Tubular Cells ◽  
Induced Apoptosis

Ochratoxin A (OTA), one of the major food-borne mycotoxins, impacts the health of humans and livestock by contaminating food and feed. However, the underlying mechanism of OTA nephrotoxicity remains unknown. This study demonstrated that OTA induced apoptosis through selective endoplasmic reticulum (ER) stress activation in human renal proximal tubular cells (HK-2). OTA increased ER-stress-related JNK and precursor caspase-4 cleavage apoptotic pathways. Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Our results demonstrate that OTA induced ER stress-related apoptosis through an ROS-mediated pathway. This study provides new evidence to clarify the mechanism of OTA-induced nephrotoxicity.

scholarly journals Long-Term Alteration of Reactive Oxygen Species Led to Multidrug Resistance in MCF-7 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Juan Cen ◽  
Li Zhang ◽  
Fangfang Liu ◽  
Feng Zhang ◽  
Bian-Sheng Ji
Keyword(s):  
Reactive Oxygen Species ◽  
Multidrug Resistance ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Related Factor ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Mcf 7

Reactive oxygen species (ROS) play an important role in multidrug resistance (MDR). This study aimed to investigate the effects of long-term ROS alteration on MDR in MCF-7 cells and to explore its underlying mechanism. Our study showed both long-term treatments of H2O2 and glutathione (GSH) led to MDR with suppressed iROS levels in MCF-7 cells. Moreover, the MDR cells induced by 0.1 μM H2O2 treatment for 20 weeks (MCF-7/ROS cells) had a higher viability and proliferative ability than the control MCF-7 cells. MCF-7/ROS cells also showed higher activity or content of intracellular antioxidants like glutathione peroxidase (GPx), GSH, superoxide dismutase (SOD), and catalase (CAT). Importantly, MCF-7/ROS cells were characterized by overexpression of MDR-related protein 1 (MRP1) and P-glycoprotein (P-gp), as well as their regulators NF-E2-related factor 2 (Nrf2), hypoxia-inducible factor 1 (HIF-1α), and the activation of PI3K/Akt pathway in upstream. Moreover, several typical MDR mediators, including glutathione S-transferase-π (GST-π) and c-Myc and Protein Kinase Cα (PKCα), were also found to be upregulated in MCF-7/ROS cells. Collectively, our results suggest that ROS may be critical in the generation of MDR, which may provide new insights into understanding of mechanisms of MDR.

scholarly journals Phage-Antibiotic Synergy via Delayed Lysis

2018 ◽  
Vol 84 (22) ◽  
Author(s):  
Minjin Kim ◽  
Yunyeol Jo ◽  
Yoon Jung Hwang ◽  
Hye Won Hong ◽  
Sung Sik Hong ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Host Cells ◽  
Oxygen Species ◽  
Particle Assembly ◽  
Content Type ◽  
Host Membrane ◽  
Quinolone Antibiotics ◽  
Phage Production

ABSTRACTWhen phages infect bacteria cultured in the presence of sublethal doses of antibiotics, the sizes of the phage plaques are significantly increased. This phenomenon is known as phage-antibiotic synergy (PAS). In this study, the observation of PAS was extended to a wide variety of bacterium-phage pairs using different classes of antibiotics. PAS was shown in both Gram-positive and Gram-negative bacteria. Cells stressed with β-lactam antibiotics filamented or swelled extensively, resulting in an increase in phage production. PAS was also sometimes observed in the presence of other classes of antibiotics with or without bacterial filamentation. The addition of antibiotics inducedrecAexpression in various bacteria, but arecAdeletion mutant strain ofEscherichia colialso showed filamentation and PAS in the presence of quinolone antibiotics. The phage adsorption efficiency did not change in the presence of the antibiotics when the cell surfaces were enlarged as they filamented. Increases in the production of phage DNA and mRNAs encoding phage proteins were observed in these cells, with only a limited increase in protein production. The data suggest that PAS is the product of a prolonged period of particle assembly due to delayed lysis. The increase in the cell surface area far exceeded the increase in phage holin production in the filamented host cells, leading to a relatively limited availability of intracellular holins for aggregating and forming holes in the host membrane. Reactive oxygen species (ROS) stress also led to an increased production of phages, while heat stress resulted in only a limited increase in phage production.IMPORTANCEPhage-antibiotic synergy (PAS) has been reported for a decade, but the underlying mechanism has never been vigorously investigated. This study shows the presence of PAS from a variety of phage-bacterium-antibiotic pairings. We show that increased phage production resulted directly from a lysis delay caused by the relative shortage of holin in filamented bacterial hosts in the presence of sublethal concentrations of stress-inducing substances, such as antibiotics and reactive oxygen species (ROS).

scholarly journals Protective Activity and Underlying Mechanism of Ginseng Seeds against UVB-Induced Damage in Human Fibroblasts

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 403
Author(s):  
Huijin Heo ◽  
Hana Lee ◽  
Jinwoo Yang ◽  
Jeehye Sung ◽  
Younghwa Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acids ◽  
Bioactive Compounds ◽  
Transforming Growth Factor ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Oxygen Species ◽  
Protective Activity ◽  
Skin Photoaging

Ginseng seeds are rich in phytosterols, ginsenosides, and fatty acids, and can therefore be used in skincare to delay the aging process. Ginseng seed embryo (GSE) and ginseng seed coat (GSC) were separated from ginseng seeds (Panax ginseng Meyer). This study evaluated the protective activity and underlying mechanism of GSE and GSC on UVB irradiation-induced skin photoaging using Hs68 cells. Their bioactive compounds, including phytosterols, ginsenosides, tocopherols, tocotrienols, and fatty acids were determined by HPLC and GC. The levels of reactive oxygen species, matrix metalloproteinases (MMPs), and collagen levels were measured in human dermal fibroblast cell line, Hs68 cells. The antioxidant capacity and contents of total polyphenols and flavonoids were higher in GSC than those in GSE. Linoleic acid was the major fatty acid in both GSE and GSC. GSE and GSC treatment alleviated UVB-induced increase of reactive oxygen species (ROS), matrix metalloproteinase (MMP)-1, and MMP-3, resulting in reduced collagen degradation. Increased UVB-mediated phosphorylation of mitogen activated protein kinase (MAPK) and activator protein-1 (AP-1) was inhibited by GSE and GSC treatment. Moreover, GSE and GSC effectively upregulated transforming growth factor-β (TGF-β) 1 levels. It was found that ginseng seeds regulate the expression of TGF-β/Smad and MAPK/AP-1 pathways. Ginseng seeds contain various bioactive compounds and have protective activity against UVB-induced skin photoaging. Therefore, ginseng seeds have the potential for use in cosmeceutical preparations.

A Comprehensive Review of Oxidative Stress as the Underlying Mechanism in Atherosclerosis and the Inefficiency of Antioxidants to Revert this Process

2019 ◽  
Vol 24 (40) ◽  
pp. 4705-4710 ◽  
Author(s):  
Kevin G. Cabezas ◽  
Carmen R. Gómez-Fernandez ◽  
Roberto Vazquez-Padron
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Plaque Formation ◽  
Oxygen Species ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase

Background: Cardiovascular diseases account for the highest mortality rate in the United States. The major underlying mechanism driving the onset and maintenance of cardiovascular diseases is atherosclerosis. Atherosclerosis is a chronic disease affecting large and medium-size arteries; it proceeds through four main stages along different decades of life, beginning at birth. Atherosclerosis is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted. Failure of intrinsic antioxidants and prophylactic antioxidant supplements to prevent atherosclerosis formation is an ongoing area of research in the race to avert, manage and cure atherosclerosis. Methods: The purpose of this work was to elucidate the actions of reactive oxygen species and oxidative stress on the formation of atherosclerosis as well as the different stages of atherosclerosis and the different mechanisms to prevent it. Through an extensive review of scientific literature, this paper correlates cell damage caused by oxidative stress to atheromatous plaque formation, as well as an in-depth analysis of high-density lipoproteins and enzymatic and non-enzymatic antioxidant role on atherosclerosis prevention. The antioxidant mechanism is overwhelmed by atherosclerotic processes and fails to be the ideal treatment of atherosclerosis. There is no scientific data that correlates prophylactic and non-prophylactic antioxidant treatment to a decrease in mortality or comorbidities pertaining to atherosclerosis. This is thought to be due to lack of consensus of optimal therapeutic doses, lack of reliable markers indicating which patient is to benefit from therapy and the chemical complexity of antioxidants in vivo. Current treatments for atherosclerosis include HMG-CoA reductase inhibitors which directly target low-density lipoproteins to tackle atherosclerotic plaque formation. Conclusion: HMG-CoA reductase inhibitors are not enough for the treatment of atherosclerosis given the complexity of the disease which has immune, musculoskeletal, genetic and hematologic aspects besides the involvement of lipids and lipoproteins. Therefore, other pharmacologic targets such as the PCSK9 enzyme and NFK- β should be researched in depth as possible treatments for atherosclerosis.

scholarly journals Deoxyelephantopin Induces Reactive Oxygen Species-Mediated Apoptosis and Autophagy in Human Osteosarcoma Cells

2017 ◽  
Vol 42 (5) ◽  
pp. 1812-1821 ◽  
Author(s):  
Jilong Zou ◽  
Yan Zhang ◽  
Jiabing Sun ◽  
Xiaoyan Wang ◽  
Hualei Tu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
Morphological Changes ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Underlying Mechanism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma Cells

Background/Aims: Osteosarcoma is the predominant form of primary bone malignancy. Although the combinational application of neoadjuvant chemotherapy and surgical resection significantly increases the survival rate, the therapeutic outcome remains unsatisfactory. Deoxyelephantopin (DET), an active ingredient of Elephantopus scaber, has been reported to have an anti-tumor effect in recent publications. This study aimed to investigate whether DET has antineoplastic effects on osteosarcoma cells and its underlying mechanism. Methods: Cell viability and morphological changes were assessed by MTT and Live/dead assays. Cell apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential were detected utilizing Annexin V-FITC/PI double staining, DCFH-DA and JC-1 probes, respectively. Autophagy was detected by mRFP-GFP-LC3 adenovirus transfection and western blot. Results: DET dose-dependently reduced the viability of osteosarcoma cells following the increase in intracellular ROS levels. Pretreatment with N-acetylcysteine (NAC) reversed this effect. Furthermore, DET induced mitochondrial apoptosis. Depolarized cells were increased, and apoptosis-related proteins, such as Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3 and cleaved ploy ADP-ribose polymerase, were activated. Additionally, we found that DET could induce autophagy in osteosarcoma cells, but autophagy inhibition did not affect the decrease in cell viability. Conclusion: DET induced apoptosis in osteosarcoma cells through ROS generation, mitochondrial dysfunction and caspase activation; in addition, autophagy was involved in the effects of DET on osteosarcoma cells.

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