Concanavalin A induces apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells
dc.authorid | Kacar, Sedat/0000-0002-0671-8529 | |
dc.authorid | kar, fatih/0000-0001-8356-9806 | |
dc.authorid | SAHINTURK, VAROL/0000-0003-2317-3644 | |
dc.authorid | Hacioglu, Ceyhan/0000-0002-0993-6118 | |
dc.authorwosid | Kacar, Sedat/I-2544-2019 | |
dc.authorwosid | kar, fatih/AAN-4285-2021 | |
dc.authorwosid | kar, fatih/AAI-4540-2021 | |
dc.authorwosid | SAHINTURK, VAROL/V-5195-2017 | |
dc.contributor.author | Kar, Fatih | |
dc.contributor.author | Kacar, Sedat | |
dc.contributor.author | Hacioglu, Ceyhan | |
dc.contributor.author | Kanbak, Gungor | |
dc.contributor.author | Sahinturk, Varol | |
dc.date.accessioned | 2021-12-01T18:49:30Z | |
dc.date.available | 2021-12-01T18:49:30Z | |
dc.date.issued | 2021 | |
dc.department | [Belirlenecek] | en_US |
dc.description.abstract | Glioma is the most common brain tumor. C6 rat glioblastoma cells provide the possibility to the scientist to study brain cancer. Concanavalin A (Con A) has a lot of antitumoral effects, especially over oxidative stress. In the present study, it was aimed to decide the impacts of various doses of Con A on C6 glioblastoma cells regarding cytotoxicity, thiol/disulfide homeostasis, apoptosis, and inflammation. We detected the cytotoxic activity of Con A (from 7.8 to 500 mu g/ml) in C6 cells by utilizing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and determined the toxic concentration of Con A. Once the optimal doses were found, the thiol-disulfide homeostasis, levels of total antioxidant and oxidant status (TAS and TOS), malondialdehyde (MDA) and glutathione (GSH), pro-inflammatory cytokines as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), apoptotic proteins as cytochrome c (CYCS), and caspase 3 (CASP3) were measured. Apoptotic and morphological changes in the C6 cells were examined with an inverted microscope and flow cytometry technique. Dose-dependent Con A triggered oxidative damage in the C6 cells, affecting the inflammatory pathway, so reducing proliferation with apoptotic proteins and morphological changes. But especially, Con A increased disulfide formation by disrupting the thiol/disulfide balance in C6 cells. This study revealed that Con A, known as carbohydrate-binding protein, generated oxidative damage, inflammation, and apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells. | en_US |
dc.description.sponsorship | Commission of Scientific Research Projects of Eskisehir Osmangazi University, Eskisehir, Turkey [2019-1915] | en_US |
dc.description.sponsorship | This study was supported by the Commission of Scientific Research Projects of Eskisehir Osmangazi University, Eskisehir, Turkey, with the grant numbers: 2019-1915. | en_US |
dc.identifier.doi | 10.1002/jbt.22742 | |
dc.identifier.issn | 1095-6670 | |
dc.identifier.issn | 1099-0461 | |
dc.identifier.issue | 5 | en_US |
dc.identifier.scopus | 2-s2.0-85100988754 | en_US |
dc.identifier.scopusquality | Q2 | en_US |
dc.identifier.uri | https://doi.org/10.1002/jbt.22742 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12684/10733 | |
dc.identifier.volume | 35 | en_US |
dc.identifier.wos | WOS:000619382000001 | en_US |
dc.identifier.wosquality | Q2 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.language.iso | en | en_US |
dc.publisher | Wiley | en_US |
dc.relation.ispartof | Journal Of Biochemical And Molecular Toxicology | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | brain tumor | en_US |
dc.subject | cancer | en_US |
dc.subject | cell death | en_US |
dc.subject | concanavalin A | en_US |
dc.subject | cytotoxicity | en_US |
dc.subject | oxidative stress | en_US |
dc.title | Concanavalin A induces apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells | en_US |
dc.type | Article | en_US |
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