{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T10:41:00Z","timestamp":1767177660252,"version":"build-2238731810"},"update-to":[{"DOI":"10.1371\/journal.pntd.0012612","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2024,11,25]],"date-time":"2024-11-25T00:00:00Z","timestamp":1732492800000}}],"reference-count":26,"publisher":"Public Library of Science (PLoS)","issue":"11","license":[{"start":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T00:00:00Z","timestamp":1730937600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior Brasil (CAPES) \u2013 UFRJ - Instituto de Microbiologia Paulo de G\u00f3es\/UFRJ"},{"name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico, CNPq","award":["CNPq1A"],"award-info":[{"award-number":["CNPq1A"]}]},{"name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico, CNPq","award":["CNPq1B"],"award-info":[{"award-number":["CNPq1B"]}]},{"name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico, CNPq","award":["CNPq 1C"],"award-info":[{"award-number":["CNPq 1C"]}]},{"name":"Funda\u00e7\u00e3o Carlos Chagas Filho de Amparo \u00e0 Pesquisa do Rio de Janeiro FAPERJ","award":["PROCESSO E-26\/ E-26\/010.02425\/2019 FAPERJ\/RJ"],"award-info":[{"award-number":["PROCESSO E-26\/ E-26\/010.02425\/2019 FAPERJ\/RJ"]}]}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:p>\n                    Oxidative stress promotes\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>cruzi<\/jats:italic>\n                    growth and development of chronic Chagas heart dysfunction. However, the literature contains gaps that must be fulfilled, largely due to variations in parasite DTU sources, cell types, mouse strains, and tools to manipulate redox status. We assessed the impact of oxidative environment on parasite burden in cardiomyoblasts and the effects of the Nrf2-inducer COPP on heart function in BALB\/c mice infected with either DTU-II Y or DTU-I Colombian\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>cruzi<\/jats:italic>\n                    strains. Treatment with antioxidants CoPP, apocynin, resveratrol, and tempol reduced parasite burden in cardiomyoblasts H9C2 for both DTUI- and II-strains, while H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    increased it. CoPP treatment improved electrical heart function when administered during acute stage of Y-strain infection, coinciding with an overall trend towards increased survival and reduced heart parasite burden. These beneficial effects surpassed those of trypanocidal benznidazole, implying that CoPP directly affects heart physiology. CoPP treatment had beneficial impact on heart systolic function when performed during acute and evaluated during chronic stage. No impact of CoPP on heart parasite burden, electrical, or mechanical function was observed during the chronic stage of Colombian-strain infection, despite previous demonstrations of improvement with other antioxidants. Treatment with CoPP also did not improve heart function of mice chronically infected with Y-strain. Our findings indicate that amastigote growth is responsive to changes in oxidative environment within heart cells regardless of the DTU source, but CoPP influence on heart parasite burden in vivo and heart function is mostly confined to the acute phase. The nature of the antioxidant employed,\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>cruzi<\/jats:italic>\n                    DTU, and the stage of disease, emerge as crucial factors to consider in heart function studies.\n                  <\/jats:p>","DOI":"10.1371\/journal.pntd.0012612","type":"journal-article","created":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T13:43:57Z","timestamp":1730987037000},"page":"e0012612","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":3,"title":["Heart function enhancement by an Nrf2-activating antioxidant in acute Y-strain Chagas disease, but not in chronic Colombian or Y-strain"],"prefix":"10.1371","volume":"18","author":[{"given":"Hilton Ant\u00f4nio","family":"Mata-Santos","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Camila Vict\u00f3ria","family":"Sousa Oliveira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel F.","family":"Feijo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel Figueiredo","family":"Vanzan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Glaucia","family":"Vilar-Pereira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Isalira P.","family":"Ramos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vitor Coutinho","family":"Carneiro","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oscar","family":"Moreno-Loaiza","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jaline Coutinho","family":"Silverio","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseli","family":"Lannes-Vieira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emiliano","family":"Medei","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcelo T.","family":"Bozza","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5605-3572","authenticated-orcid":true,"given":"Claudia N.","family":"Paiva","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"340","published-online":{"date-parts":[[2024,11,7]]},"reference":[{"issue":"4","key":"pntd.0012612.ref001","doi-asserted-by":"crossref","first-page":"e1006928","DOI":"10.1371\/journal.ppat.1006928","article-title":"ROS and Trypanosoma cruzi: Fuel to infection, poison to the heart","volume":"14","author":"CN Paiva","year":"2018","journal-title":"PLoS Pathog"},{"issue":"7","key":"pntd.0012612.ref002","doi-asserted-by":"crossref","first-page":"2531","DOI":"10.1172\/JCI58525","article-title":"Oxidative stress fuels Trypanosoma cruzi infection in mice","volume":"122","author":"CN Paiva","year":"2012","journal-title":"J Clin Invest"},{"issue":"6","key":"pntd.0012612.ref003","doi-asserted-by":"crossref","first-page":"1000","DOI":"10.1089\/ars.2013.5447","article-title":"Are reactive oxygen species always detrimental to pathogens?","volume":"20","author":"CN Paiva","year":"2014","journal-title":"Antioxid Redox Signal"},{"issue":"4","key":"pntd.0012612.ref004","doi-asserted-by":"crossref","first-page":"e0004555","DOI":"10.1371\/journal.pntd.0004555","article-title":"Trypanosoma cruzi Needs a Signal Provided by Reactive Oxygen Species to Infect Macrophages","volume":"10","author":"GR Goes","year":"2016","journal-title":"PLoS Negl Trop Dis"},{"issue":"6","key":"pntd.0012612.ref005","doi-asserted-by":"crossref","first-page":"e2279","DOI":"10.1371\/journal.pntd.0002279","article-title":"Oxidative stress and DNA lesions: the role of 8-oxoguanine lesions in Trypanosoma cruzi cell viability","volume":"7","author":"PH Aguiar","year":"2013","journal-title":"PLoS Negl Trop Dis"},{"issue":"10","key":"pntd.0012612.ref006","doi-asserted-by":"crossref","first-page":"e25935","DOI":"10.1371\/journal.pone.0025935","article-title":"Heme-induced ROS in Trypanosoma cruzi activates CaMKII-like that triggers epimastigote proliferation. 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