scholarly journals Nitroxide TEMPO: A genotoxic and oxidative stress inducer in cultured cells

2013 ◽  
Vol 27 (5) ◽  
pp. 1496-1502 ◽  
Author(s):  
Xiaoqing Guo ◽  
Roberta A. Mittelstaedt ◽  
Lei Guo ◽  
Joseph G. Shaddock ◽  
Robert H. Heflich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cultured Cells ◽  
And Oxidative Stress ◽  
Oxidative Stress Inducer

Action of 6-amino-3-pyridinols as novel antioxidants against free radicals and oxidative stress in solution, plasma, and cultured cells

2010 ◽  
Vol 48 (10) ◽  
pp. 1358-1365 ◽  
Author(s):  
Yo Omata ◽  
Yoshiro Saito ◽  
Yasukazu Yoshida ◽  
Byeong-Seon Jeong ◽  
Remigiusz Serwa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Cultured Cells ◽  
Novel Antioxidants ◽  
And Oxidative Stress

scholarly journals MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

2019 ◽  
Vol 20 (20) ◽  
pp. 5200 ◽  
Author(s):  
Cheleschi ◽  
Gallo ◽  
Barbarino ◽  
Giannotti ◽  
Mondanelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Structural Damage ◽  
Cultured Cells ◽  
B Cell Lymphoma ◽  
Synovial Fibroblasts ◽  
Type Ii Collagen ◽  
Superoxide Production ◽  
Nuclear Factor ◽  
Regulated Gene Expression ◽  
And Oxidative Stress

Synovial membrane inflammation actively participate to structural damage during osteoarthritis (OA). Adipokines, miRNA, and oxidative stress contribute to synovitis and cartilage destruction in OA. We investigated the relationship between visfatin, resistin and miRNA in oxidative stress regulation, in human OA synovial fibroblasts. Cultured cells were treated with visfatin and resistin. After 24 h, we evaluated various pro-inflammatory cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma (BCL)2 by qRT-PCR, apoptosis and mitochondrial superoxide production by cytometry, p50 nuclear factor (NF)-κB by immunofluorescence. Synoviocytes were transfected with miRNA inhibitors and oxidative stress evaluation after adipokines stimulus was performed. The implication of NF-κB pathway was assessed by the use of a NF-κB inhibitor (BAY-11-7082). Visfatin and resistin significantly up-regulated gene expression of interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factor (TNF)-α, MMP-1, MMP-13 and reduced Col2a1. Furthermore, adipokines induced apoptosis and superoxide production, the transcriptional levels of BCL2, superoxide dismutase (SOD)-2, catalase (CAT), nuclear factor erythroid 2 like 2 (NRF2), miR-34a, miR-146a, and miR-181a. MiRNA inhibitors counteracted adipokines modulation of oxidative stress. Visfatin and resistin effects were suppressed by BAY-11-7082. Our data suggest that miRNA may represent possible mediators of oxidative stress induced by visfatin and resistin via NF-κB pathway in human OA synoviocytes.

scholarly journals Extensive Thiol Profiling for Assessment of Intracellular Redox Status in Cultured Cells by HPLC-MS/MS

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 24
Author(s):  
Jiandong Wu ◽  
Anna Chernatynskaya ◽  
Annalise Pfaff ◽  
Huari Kou ◽  
Nan Cen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Defense Mechanisms ◽  
High Performance ◽  
Cultured Cells ◽  
Redox Status ◽  
Oxidative Stress Responses ◽  
Sulfur Containing ◽  
And Oxidative Stress ◽  
Oxidative Insult

Oxidative stress may contribute to the pathology of many diseases, and endogenous thiols, especially glutathione (GSH) and its metabolites, play essential roles in the maintenance of normal redox status. Understanding how these metabolites change in response to oxidative insult can provide key insights into potential methods of prevention and treatment. Most existing methodologies focus only on the GSH/GSH disulfide (GSSG) redox couple, but GSH regulation is highly complex and depends on several pathways with multiple redox-active sulfur-containing species. In order to more fully characterize thiol redox status in response to oxidative insult, a high-performance liquid chromatography with tandem mass spectrometry (HPLC-MS/MS) method was developed to simultaneously determine seven sulfur-containing metabolites, generating a panel that systematically examines several pathways involved in thiol metabolism and oxidative stress responses. The sensitivity (LOQ as low as 0.01 ng/mL), accuracy (88–126% spike recovery), and precision (≤12% RSD) were comparable or superior to those of existing methods. Additionally, the method was used to compare the baseline thiol profiles and oxidative stress responses of cell lines derived from different tissues. The results revealed a previously unreported response to oxidative stress in lens epithelial (B3) cells, which may be exploited as a new therapeutic target for oxidative-stress-related ocular diseases. Further application of this method may uncover new pathways involved in oxidative-stress-related diseases and endogenous defense mechanisms.

Plasma membrane oxidoreductase activity in cultured cells in relation to mitochondrial function and oxidative stress

BioFactors ◽  
2004 ◽  
Vol 20 (4) ◽  
pp. 265-272 ◽  
Author(s):  
Giulia Deleonardi ◽  
Annalisa Biondi ◽  
Marilena D'Aurelio ◽  
Milena Merlo Pich ◽  
Karmen Stankov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Mitochondrial Function ◽  
Cultured Cells ◽  
Oxidoreductase Activity ◽  
And Oxidative Stress

scholarly journals Downregulation of miR-128 Ameliorates Ang II-Induced Cardiac Remodeling via SIRT1/PIK3R1 Multiple Targets

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Heqin Zhan ◽  
Feng Huang ◽  
Qian Niu ◽  
Mingli Jiao ◽  
Xumeng Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Cultured Cells ◽  
Ang Ii ◽  
Stress Injury ◽  
And Oxidative Stress

Recent studies reported that miR-128 was differentially expressed in cardiomyocytes in response to pathologic stress. However, its function and mechanism remain to be fully elucidated. The aim of the present study was to investigate the role of miR-128 in chronic angiotensin II (Ang II) infusion-induced cardiac remodeling and its underlying mechanism. The cardiac remodeling and heart failure in vivo were established in C57BL/6 mice by chronic subcutaneous Ang II delivery. Knocking down miR-128 was conducted in the hearts of the mice by intravenous injection of HBAAV2/9-miR-128-GFP sponge (miR-128 inhibitor). In vitro experiments of cardiac hypertrophy, apoptosis, and aberrant autophagy were performed in cultured cells after Ang II treatment or transfection of miR-128 antagomir. Our results showed that chronic Ang II delivery for 28 days induced cardiac dysfunction, hypertrophy, fibrosis, apoptosis, and oxidative stress in the mice, while the miR-128 expression was notably enhanced in the left ventricle. Silencing miR-128 in the hearts of mice ameliorated Ang II-induced cardiac dysfunction, hypertrophy, fibrosis apoptosis, and oxidative stress injury. Moreover, Ang II induced excessive autophagy in the mouse hearts, which was suppressed by miR-128 knockdown. In cultured cells, Ang II treatment induced a marked elevation in the miR-128 expression. Downregulation of miR-128 in the cells by transfection with miR-128 antagomir attenuated Ang II-induced apoptosis and oxidative injury probably via directly targeting on the SIRT1/p53 pathway. Intriguingly, we found that miR-128 inhibition activated PIK3R1/Akt/mTOR pathway and thereby significantly damped Ang II-stimulated pathological autophagy in cardiomyocytes, which consequently mitigated cell oxidative stress and apoptosis. In conclusion, downregulation of miR-128 ameliorates Ang II-provoked cardiac oxidative stress, hypertrophy, fibrosis, apoptosis, and dysfunction in mice, likely through targeting on PIK3R1/Akt/mTORC1 and/or SIRT1/p53 pathways. These results indicate that miR-128 inhibition might be a potent therapeutic strategy for maladaptive cardiac remodeling and heart failure.

scholarly journals Effects of altered zinc availability on proliferation and oxidative stress in cultured cells

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Kavitha Sankavaram ◽  
Bruce J Grattan ◽  
Robin Walker ◽  
Hea Jin Park ◽  
Hedley C Freake
Keyword(s):  
Oxidative Stress ◽  
Cultured Cells ◽  
Zinc Availability ◽  
And Oxidative Stress

scholarly journals The Ste20 kinases SPAK and OSR1 travel between cells through exosomes

2016 ◽  
Vol 311 (1) ◽  
pp. C43-C53 ◽  
Author(s):  
Rainelli Koumangoye ◽  
Eric Delpire
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Cell Biology ◽  
Culture Medium ◽  
Cultured Cells ◽  
Cell Communication ◽  
Oxidative Stress Response ◽  
Hek293 Cells ◽  
Conditioned Culture Medium ◽  
And Oxidative Stress

Proteomics studies have identified Ste20-related proline/alanine-rich kinase (SPAK) and oxidative stress response 1 (OSR1) in exosomes isolated from body fluids such as blood, saliva, and urine. Because proteomics studies likely overestimate the number of exosome proteins, we sought to confirm and extend this observation using traditional biochemical and cell biology methods. We utilized HEK293 cells in culture to verify the packaging of these Ste20 kinases in exosomes. Using a series of centrifugation and filtration steps of conditioned culture medium isolated from HEK293 cells, we isolated nanovesicles in the range of 40–100 nm. We show that these small vesicles express the tetraspanin protein CD63 and lack endoplasmic reticulum and Golgi markers, consistent with these being exosomes. We show by Western blot and immunogold analyses that these exosomes express SPAK, OSR1, and Na-K-Cl cotransporter 1 (NKCC1). We show that exosomes are not only secreted by cells, but also accumulated by adjacent cells. Indeed, exposing cultured cells to exosomes produced by other cells expressing a fluorescently labeled kinase resulted in the kinase finding its way into the cytoplasm of these cells, consistent with the idea of exosomes serving as cell-to-cell communication vessels. Similarly, coculturing cells expressing different fluorescently tagged proteins resulted in the exchange of proteins between cells. In addition, we show that both SPAK and OSR1 kinases entering cells through exosomes are preferentially expressed at the plasma membrane and that the kinases in exosomes are functional and maintain NKCC1 in a phosphorylated state.

Association between calcitriol and paricalcitol with oxidative stress in patients with hemodialysis

2020 ◽  
pp. 1-8
Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Total Oxidant Status ◽  
Vitamin D Analog ◽  
Total Antioxidant ◽  
Oxidant Status ◽  
And Oxidative Stress

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.

Sign in / Sign up

Export Citation Format

Share Document