scholarly journals ffect of Etazolate on ROS Production after tBHP-Induced Oxidative Stress in Oligodendroglial 158N Cell Line

2020 ◽  
Author(s):  
Elena Chierto ◽  
Giulia Cristinziano ◽  
Francesca Sapone ◽  
Delphine Meffre ◽  
Mehrnaz Jafarian-Tehrani
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Ros Production

Relationship between copper(ii) complexes with FomA adhesin fragments ofF. nucleatumand colorectal cancer. Coordination pattern and ability to promote ROS production

2018 ◽  
Vol 47 (15) ◽  
pp. 5445-5458 ◽  
Author(s):  
M. K. Lesiów ◽  
U. K. Komarnicka ◽  
K. Stokowa-Sołtys ◽  
K. Rolka ◽  
A. Łęgowska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Cell Line ◽  
Coordination Pattern ◽  
Ros Production ◽  
Ct26 Cell

The copper(ii) binding of the fragments of FomA was studied. Complexes stimulate the CT26 cell line to produce ROS which lead to oxidative stress.

scholarly journals Genotoxicity and oxidative stress induction by polystyrene nanoparticles in the colorectal cancer cell line HCT116

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0255120
Author(s):  
Giulia Vecchiotti ◽  
Sabrina Colafarina ◽  
Massimo Aloisi ◽  
Osvaldo Zarivi ◽  
Piero Di Carlo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Hct116 Cell ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Ros Production ◽  
Polystyrene Nanoparticles ◽  
Contaminated Food ◽  
Potential Damage ◽  
The Impact

The potential risks of environmental nanoparticles (NPs), in particular Polystyrene Nanoparticles (PNPs), is an emerging problem; specifically, the interaction of PNPs with intestinal cells has not been characterized so far. The mechanism by which polystyrene particles are transferred to humans has not yet been clarified, whether directly through ingestion from contaminated food. We evaluated the interaction between PNPs and colorectal adenocarcinoma cells (HCT116). Cells were exposed to different concentrations of PNPs, metabolic activity and the consequent cytotoxic potential were assessed through viability test; we evaluated the PNP genotoxic potential through the Cytokinesis-Block Micronucleus cytome (CBMN cyt) assay. Finally, we detected Reactive Oxygen Species (ROS) production after NPs exposure and performed Western Blot analysis to analyze the enzymes (SOD1, SOD2, Catalase, Glutathione Peroxidase) involved in the cell detoxification process that comes into play during the cell-PNPs interaction. This work analyzes the cyto and genotoxicity of PNPs in the colorectal HCT116 cell line, in particular the potential damage from oxidative stress produced by PNPs inside the cells related to the consequent nuclear damage. Our results show moderate toxicity of PNPs both in terms of ROS production and DNA damage. Further studies will be needed on different cell lines to have a more complete picture of the impact of environmental pollution on human health in terms of PNPs cytotoxicity and genotoxicity.

Lopinavir/Ritonavir Treatment Induces Oxidative Stress and Caspaseindependent Apoptosis in Human Glioblastoma U-87 MG Cell Line

2018 ◽  
Vol 16 (2) ◽  
pp. 106-112 ◽  
Author(s):  
Rossella Gratton ◽  
Paola Maura Tricarico ◽  
Rafael Lima Guimaraes ◽  
Fulvio Celsi ◽  
Sergio Crovella
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Cell Death ◽  
Side Effects ◽  
Cell Line ◽  
Apoptotic Cell ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
Human Glioblastoma ◽  
The Impact

Background:Lopinavir and Ritonavir (LPV/r) treatment is widely used to prevent HIV mother-to-child transmission. Nevertheless, studies related to the impact of these compounds on patients, in particular in the foetus and newborns, are strictly required due to the controversial findings reported in the literature concerning possible neurologic side effects following the administration of these drugs.Objectives:In our study, we evaluated the impact of LPV/r treatment on the human glioblastoma U- 87 MG cell line.Methods:In order to evaluate the influence of Lopinavir and Ritonavir in terms of oxidative stress (ROS production), mitochondrial morphology and apoptotic cell death, the latter either in the presence or in the absence of caspase-3 and -9 inhibitors, we treated U-87 MG with increasing doses (0.1-1-10-25-50 µM) of Lopinavir and Ritonavir for 24h, either in single formulation or in combination. ROS production was measured by flow cytometry using H2DCFDA dye, mitochondrial morphology was evaluated using MitoRed dye and apoptotic cell death was monitored by flow cytometry using Annexin V-FITC and Propidium Iodide.Results:We observed that co-treatment with Lopinavir and Ritonavir (25 and 50 µM) promoted a significant increase in ROS production, caused mitochondrial network damage and induced apoptosis in a caspase-independent manner.Conclusion:Based on our findings, concordant with others reported in the literature, we hypothesize that LPV/r treatment could not be entirely free from side effects, being aware of the need of validation in in vivo models, necessary to confirm our results.

Characterizing effects of excess copper levels in a human astrocytic cell line with focus on oxidative stress markers

2021 ◽  
Vol 65 ◽  
pp. 126711
Author(s):  
Barbara Witt ◽  
Michael Stiboller ◽  
Stefanie Raschke ◽  
Sharleen Friese ◽  
Franziska Ebert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Excess Copper

scholarly journals IκBα targeting promotes oxidative stress-dependent cell death

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Giovanna Carrà ◽  
Giuseppe Ermondi ◽  
Chiara Riganti ◽  
Luisella Righi ◽  
Giulia Caron ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Fate ◽  
Protein Interactions ◽  
In Silico ◽  
Inverse Correlation ◽  
Ros Production ◽  
Gene Encoding ◽  
Specific Expression ◽  
Novel Approach ◽  
Stress Dependent

Abstract Background Oxidative stress is a hallmark of many cancers. The increment in reactive oxygen species (ROS), resulting from an increased mitochondrial respiration, is the major cause of oxidative stress. Cell fate is known to be intricately linked to the amount of ROS produced. The direct generation of ROS is also one of the mechanisms exploited by common anticancer therapies, such as chemotherapy. Methods We assessed the role of NFKBIA with various approaches, including in silico analyses, RNA-silencing and xenotransplantation. Western blot analyses, immunohistochemistry and RT-qPCR were used to detect the expression of specific proteins and genes. Immunoprecipitation and pull-down experiments were used to evaluate protein-protein interactions. Results Here, by using an in silico approach, following the identification of NFKBIA (the gene encoding IκBα) amplification in various cancers, we described an inverse correlation between IκBα, oxidative metabolism, and ROS production in lung cancer. Furthermore, we showed that novel IκBα targeting compounds combined with cisplatin treatment promote an increase in ROS beyond the tolerated threshold, thus causing death by oxytosis. Conclusions NFKBIA amplification and IκBα overexpression identify a unique cancer subtype associated with specific expression profile and metabolic signatures. Through p65-NFKB regulation, IκBα overexpression favors metabolic rewiring of cancer cells and distinct susceptibility to cisplatin. Lastly, we have developed a novel approach to disrupt IκBα/p65 interaction, restoring p65-mediated apoptotic responses to cisplatin due to mitochondria deregulation and ROS-production.

scholarly journals Dibenzoylthiamine Has Powerful Antioxidant and Anti-Inflammatory Properties in Cultured Cells and in Mouse Models of Stress and Neurodegeneration

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 361
Author(s):  
Margaux Sambon ◽  
Anna Gorlova ◽  
Alice Demelenne ◽  
Judit Alhama-Riba ◽  
Bernard Coumans ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Cell Line ◽  
Mouse Models ◽  
Cultured Cells ◽  
Therapeutic Potential ◽  
Motor Dysfunction ◽  
Oxidative Stress Marker ◽  
Bv2 Cells ◽  
Anti Inflammatory

Thiamine precursors, the most studied being benfotiamine (BFT), have protective effects in mouse models of neurodegenerative diseases. BFT decreased oxidative stress and inflammation, two major characteristics of neurodegenerative diseases, in a neuroblastoma cell line (Neuro2a) and an immortalized brain microglial cell line (BV2). Here, we tested the potential antioxidant and anti-inflammatory effects of the hitherto unexplored derivative O,S-dibenzoylthiamine (DBT) in these two cell lines. We show that DBT protects Neuro2a cells against paraquat (PQ) toxicity by counteracting oxidative stress at low concentrations and increases the synthesis of reduced glutathione and NADPH in a Nrf2-independent manner. In BV2 cells activated by lipopolysaccharides (LPS), DBT significantly decreased inflammation by suppressing translocation of NF-κB to the nucleus. Our results also demonstrate the superiority of DBT over thiamine and other thiamine precursors, including BFT, in all of the in vitro models. Finally, we show that the chronic administration of DBT arrested motor dysfunction in FUS transgenic mice, a model of amyotrophic lateral sclerosis, and it reduced depressive-like behavior in a mouse model of ultrasound-induced stress in which it normalized oxidative stress marker levels in the brain. Together, our data suggest that DBT may have therapeutic potential for brain pathology associated with oxidative stress and inflammation by novel, coenzyme-independent mechanisms.

Glycine alleviates fluoride‐induced oxidative stress, apoptosis and senescence in a porcine testicular Sertoli cell line

2021 ◽  
Author(s):  
Ying Liu ◽  
Boxing Sun ◽  
Shaoxuan Zhang ◽  
Jing Li ◽  
Jiajia Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Sertoli Cell ◽  
Sertoli Cell Line

scholarly journals Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation

2021 ◽  
Vol 22 (3) ◽  
pp. 1146
Author(s):  
Reinhard Ullmann ◽  
Benjamin Valentin Becker ◽  
Simone Rothmiller ◽  
Annette Schmidt ◽  
Horst Thiermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Copy Number ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Chromosomal Translocations ◽  
Dna Copy Number ◽  
Mutational Signatures ◽  
Copy Number Changes ◽  
And Oxidative Stress

Sulfur mustard (SM) is a chemical warfare agent that can damage DNA via alkylation and oxidative stress. Because of its genotoxicity, SM is cancerogenic and the progenitor of many chemotherapeutics. Previously, we developed an SM-resistant cell line via chronic exposure of the popular keratinocyte cell line HaCaT to increasing doses of SM over a period of 40 months. In this study, we compared the genomic landscape of the SM-resistant cell line HaCaT/SM to its sensitive parental line HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array Comparative Genomic Hybridization (array CGH), employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations, and derived mutational signatures by whole-genome sequencing. We observed that chronic SM exposure eliminated the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability toward genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double-strand breaks and their misrepair. HaCaT/SM-specific single-nucleotide variants showed enrichment of C > A and T > A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology, this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

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