{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T21:48:04Z","timestamp":1789422484079,"version":"build-2803163510"},"reference-count":81,"publisher":"Public Library of Science (PLoS)","issue":"5","license":[{"start":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T00:00:00Z","timestamp":1715299200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"C.N.R.S."},{"name":"I.N.S.E.R.M."}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS ONE"],"abstract":"<jats:p>\n                    Although the toxicity of arsenic depends on its chemical forms, few studies have taken into account the ambiguous phenomenon that sodium arsenite (NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    ) acts as a potent carcinogen while arsenic trioxide (ATO, As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    ) serves as an effective therapeutic agent in lymphoma, suggesting that NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    and As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    may act via paradoxical ways to either promote or inhibit cancer pathogenesis. Here, we compared the cellular response of the two arsenical compounds, NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    and As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    , on the Burkitt lymphoma cell model, the Epstein Barr Virus (EBV)-positive P3HR1 cells. Using flow cytometry and biochemistry analyses, we showed that a NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    treatment induces P3HR1 cell death, combined with drastic drops in \u0394\u03a8m, NAD(P)H and ATP levels. In contrast, As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    -treated cells resist to cell death, with a moderate reduction of \u0394\u03a8m, NAD(P)H and ATP. While both compounds block cells in G2\/M and affect their protein carbonylation and lipid peroxidation, As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    induces a milder increase in superoxide anions and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    than NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    , associated to a milder inhibition of antioxidant defenses. By electron microscopy, RT-qPCR and image cytometry analyses, we showed that As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    -treated cells display an overall autophagic response, combined with mitophagy and an unfolded protein response, characteristics that were not observed following a NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    treatment. As previous works showed that As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    reactivates EBV in P3HR1 cells, we treated the EBV\n                    <jats:sup>-<\/jats:sup>\n                    Ramos-1 cells and showed that autophagy was not induced in these EBV\n                    <jats:sup>-<\/jats:sup>\n                    cells upon As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    treatment suggesting that the boost of autophagy observed in As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    -treated P3HR1 cells could be due to the presence of EBV in these cells. Overall, our results suggest that As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    is an autophagic inducer which action is enhanced when EBV is present in the cells, in contrast to NaAsO\n                    <jats:sub>2<\/jats:sub>\n                    , which induces cell death. That\u2019s why As\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>3<\/jats:sub>\n                    is combined with other chemicals, as all-trans retinoic acid, to better target cancer cells in therapeutic treatments.\n                  <\/jats:p>","DOI":"10.1371\/journal.pone.0302701","type":"journal-article","created":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T13:25:23Z","timestamp":1715347523000},"page":"e0302701","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":10,"title":["Sodium arsenite and arsenic trioxide differently affect the oxidative stress of lymphoblastoid cells: An intricate crosstalk between mitochondria, autophagy and cell death"],"prefix":"10.1371","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7473-2229","authenticated-orcid":true,"given":"Nathan Earl","family":"Rainey","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne-Sophie","family":"Armand","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrice X.","family":"Petit","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2024,5,10]]},"reference":[{"issue":"1","key":"pone.0302701.ref001","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S0378-4274(02)00084-X","article-title":"Arsenic toxicity and potential mechanisms of action","volume":"133","author":"MF Hughes","year":"2002","journal-title":"Toxicol Lett"},{"issue":"2","key":"pone.0302701.ref002","doi-asserted-by":"crossref","first-page":"305","DOI":"10.1093\/toxsci\/kfr184","article-title":"Arsenic exposure and toxicology: a historical perspective","volume":"123","author":"MF Hughes","year":"2011","journal-title":"Toxicol Sci"},{"issue":"14","key":"pone.0302701.ref003","first-page":"3893","article-title":"Mechanisms of action of arsenic trioxide","volume":"62","author":"WH Miller","year":"2002","journal-title":"Cancer Res"},{"key":"pone.0302701.ref004","doi-asserted-by":"crossref","first-page":"325","DOI":"10.1016\/B978-0-12-394390-3.00012-4","article-title":"Pathways of arsenic uptake and efflux","volume":"69","author":"HC Yang","year":"2012","journal-title":"Curr Top Membr"},{"issue":"2","key":"pone.0302701.ref005","doi-asserted-by":"crossref","first-page":"505","DOI":"10.1128\/jb.131.2.505-511.1977","article-title":"Two systems for the uptake of phosphate in Escherichia coli","volume":"131","author":"H Rosenberg","year":"1977","journal-title":"J Bacteriol"},{"issue":"1","key":"pone.0302701.ref006","doi-asserted-by":"crossref","first-page":"43","DOI":"10.1007\/s00005-012-0205-y","article-title":"Autophagy, apoptosis, mitoptosis and necrosis: interdependence between those pathways and effects on cancer","volume":"61","author":"W Chaabane","year":"2013","journal-title":"Arch Immunol Ther Exp (Warsz)"},{"key":"pone.0302701.ref007","doi-asserted-by":"crossref","first-page":"260146","DOI":"10.1155\/2008\/260146","article-title":"Arsenic-based antineoplastic drugs and their mechanisms of action","volume":"2008","author":"SJ Ralph","year":"2008","journal-title":"Met Based Drugs"},{"key":"pone.0302701.ref008","doi-asserted-by":"crossref","first-page":"243","DOI":"10.1146\/annurev.pharmtox.47.120505.105144","article-title":"Arsenic: signal transduction, transcription factor, and biotransformation involved in cellular response and toxicity","volume":"47","author":"Y Kumagai","year":"2007","journal-title":"Annu Rev Pharmacol Toxicol"},{"issue":"10","key":"pone.0302701.ref009","doi-asserted-by":"crossref","first-page":"3365","DOI":"10.1128\/jb.179.10.3365-3367.1997","article-title":"Antimonite is accumulated by the glycerol facilitator GlpF in Escherichia coli","volume":"179","author":"OI Sanders","year":"1997","journal-title":"J Bacteriol"},{"issue":"1\u20132","key":"pone.0302701.ref010","doi-asserted-by":"crossref","first-page":"67","DOI":"10.1023\/B:MCBI.0000007262.26044.e8","article-title":"Oxidative mechanism of arsenic toxicity and carcinogenesis","volume":"255","author":"H Shi","year":"2004","journal-title":"Mol Cell Biochem"},{"issue":"Suppl 2","key":"pone.0302701.ref011","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1634\/theoncologist.6-suppl_2-3","article-title":"History of the development of arsenic derivatives in cancer therapy","volume":"6","author":"S Waxman","year":"2001","journal-title":"Oncologist"},{"issue":"3","key":"pone.0302701.ref012","doi-asserted-by":"crossref","first-page":"309","DOI":"10.1111\/j.1365-2141.2009.07623.x","article-title":"Notoriety to respectability: a short history of arsenic prior to its present day use in haematology","volume":"145","author":"D. 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