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dc.contributor.authorTronci, Laura
dc.contributor.authorSerreli, Gabriele
dc.contributor.authorPiras, Cristina
dc.contributor.authorFrau, Daniela Virginia
dc.contributor.authorDettori, Tinuccia
dc.contributor.authorDeiana, Monica
dc.contributor.authorMurgia, Federica
dc.contributor.authorSantoru, Maria Laura
dc.contributor.authorSpada, Martina
dc.contributor.authorLeoni, Vera Piera
dc.contributor.authorGriffin, Julian Leether
dc.contributor.authorVanni, Roberta
dc.contributor.authorAtzori, Luigi
dc.contributor.authorCaria, Paola
dc.date.accessioned2021-07-07T13:59:19Z
dc.date.available2021-07-07T13:59:19Z
dc.date.issued2021-05-20
dc.identifier.citationAntioxidants (Basel, Switzerland), volume 10, issue 5
dc.identifier.issn2076-3921
dc.identifier.otherPMC8161084
dc.identifier.other34065197
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/324848
dc.description.abstractHigh-dose of vitamin C (L-ascorbic acid, ascorbate) exhibits anti-tumoral effects, primarily mediated by pro-oxidant mechanisms. This cytotoxic effect is thought to affect the reciprocal crosstalk between redox balance and cell metabolism in different cancer types. Vitamin C also inhibits the growth of papillary thyroid carcinoma (PTC) cells, although the metabolic and redox effects remain to be fully understood. To shed light on these aspects, PTC-derived cell lines harboring the most common genetic alterations characterizing this tumor were used. Cell viability, apoptosis, and the metabolome were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test (MTT), flow cytometry, and UHPLC/MS. Changes were observed in redox homeostasis, with increased reactive oxygen species (ROS) level and perturbation in antioxidants and electron carriers, leading to cell death by both apoptosis and necrosis. The oxidative stress contributed to the metabolic alterations in both glycolysis and TCA cycle. Our results confirm the pro-oxidant effect of vitamin C as relevant in triggering the cytotoxicity in PTC cells and suggest that inhibition of glycolysis and alteration of TCA cycle via NAD<sup>+</sup> depletion can play an important role in this mechanism of PTC cancer cell death.
dc.languageeng
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceessn: 2076-3921
dc.sourcenlmid: 101668981
dc.subjectAntioxidants
dc.subjectVitamin C
dc.subjectCell metabolism
dc.subjectROS
dc.subjectTCA cycle
dc.subjectAnticancer effects
dc.subjectglycolysis
dc.subjectPtc Cells
dc.titleVitamin C Cytotoxicity and Its Effects in Redox Homeostasis and Energetic Metabolism in Papillary Thyroid Carcinoma Cell Lines.
dc.typeArticle
dc.date.updated2021-07-07T13:59:18Z
dc.identifier.doi10.17863/CAM.72302
rioxxterms.versionofrecord10.3390/antiox10050809
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidTronci, Laura [0000-0002-1217-4046]
dc.contributor.orcidSerreli, Gabriele [0000-0002-1971-3989]
dc.contributor.orcidPiras, Cristina [0000-0003-0750-4837]
dc.contributor.orcidDeiana, Monica [0000-0002-7166-1856]
dc.contributor.orcidVanni, Roberta [0000-0003-1367-5958]
dc.contributor.orcidAtzori, Luigi [0000-0002-0606-4959]


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International