{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang ZZ"],"funding":["Burroughs Wellcome Fund","NHLBI NIH HHS","NCI NIH HHS","National Institutes of Health","NIAMS NIH HHS"],"pagination":["22861-22867"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5087709"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["291(44)"],"pubmed_abstract":["The discovery that oxidized vitamin C, dehydroascorbate (DHA), can induce oxidative stress and cell death in cancer cells has rekindled interest in the use of high dose vitamin C (VC) as a cancer therapy. However, high dose VC has shown limited efficacy in clinical trials, possibly due to the decreased bioavailability of oral VC. Because human erythrocytes express high levels of Glut1, take up DHA, and reduce it to VC, we tested how erythrocytes might impact high dose VC therapies. Cancer cells are protected from VC-mediated cell death when co-cultured with physiologically relevant numbers of erythrocytes. Pharmacological doses of VC induce oxidative stress, GSH depletion, and increased glucose flux through the oxidative pentose phosphate pathway (PPP) in erythrocytes. Incubation of erythr"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Glutathione Depletion, Pentose Phosphate Pathway Activation, and Hemolysis in Erythrocytes Protecting Cancer Cells from Vitamin C-induced Oxidative Stress."],"pmcid":["PMC5087709"],"funding_grant_id":["K23 HL132054","K08 CA164047","K23 AR069728","R01 CA157996","CAMS 1010978"],"pubmed_authors":["Zhang ZZ","Glass D","Deberardinis RJ","Zia A","Lee EE","Sudderth J","Yue Y","Wang RC"],"additional_accession":[]},"is_claimable":false,"name":"Glutathione Depletion, Pentose Phosphate Pathway Activation, and Hemolysis in Erythrocytes Protecting Cancer Cells from Vitamin C-induced Oxidative Stress.","description":"The discovery that oxidized vitamin C, dehydroascorbate (DHA), can induce oxidative stress and cell death in cancer cells has rekindled interest in the use of high dose vitamin C (VC) as a cancer therapy. However, high dose VC has shown limited efficacy in clinical trials, possibly due to the decreased bioavailability of oral VC. Because human erythrocytes express high levels of Glut1, take up DHA, and reduce it to VC, we tested how erythrocytes might impact high dose VC therapies. Cancer cells are protected from VC-mediated cell death when co-cultured with physiologically relevant numbers of erythrocytes. Pharmacological doses of VC induce oxidative stress, GSH depletion, and increased glucose flux through the oxidative pentose phosphate pathway (PPP) in erythrocytes. Incubation of erythr","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Oct","modification":"2025-04-22T08:55:20.234Z","creation":"2019-03-27T02:27:53Z"},"accession":"S-EPMC5087709","cross_references":{"pubmed":["27660392"],"doi":["10.1074/jbc.C116.748848","10.1074/jbc.c116.748848"]}}