Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/342739
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampTamarindo, Guilherme Henrique-
dc.contributor.authorunicampGadelha, Fernanda Ramos-
dc.typeArtigopt_BR
dc.titleMelatonin and docosahexaenoic acid decrease proliferation of PNT1A prostate benign cells via modulation of mitochondrial bioenergetics and ROS productionpt_BR
dc.contributor.authorTamarindo, Guilherme H.-
dc.contributor.authorRibeiro, Daniele L.-
dc.contributor.authorGobbo, Marina G.-
dc.contributor.authorGuerra, Luiz H. A.-
dc.contributor.authorRahal, Paula-
dc.contributor.authorTaboga, Sebastiao R.-
dc.contributor.authorGadelha, Fernanda R.-
dc.contributor.authorGoes, Rejane M.-
dc.subjectNeoplasias da próstatapt_BR
dc.subjectMelatoninapt_BR
dc.subjectÁcido docosahexaenoicopt_BR
dc.subject.otherlanguageProstatic neoplasmspt_BR
dc.subject.otherlanguageMelatoninpt_BR
dc.subject.otherlanguageDocosahexaenoic acidpt_BR
dc.description.abstractProstate cancer development has been associated with changes in mitochondria' activity and reactive oxygen species (ROS) production. Melatonin (MLT) and docosahexaenoic acid (DHA) have properties to modulate both, but their protective role, mainly at early stages of prostate cancer, remains unclear. In this study, the effects of MLT and DHA, combined or not, on PNT1A cells with regard to mitochondria bioenergetics, ROS production, and proliferation-related pathways were examined. Based on dose response and lipid accumulation assays, DHA at 100 mu M and MLT at 1 mu M for 48 h were chosen. DHA doubled and MLT reduced (40%) superoxide anion production, but coincubation (DM) did not normalize to control. Hydrogen peroxide production decreased after MLT incubation only (p < 0.01). These alterations affected the area and perimeter of mitochondria, since DHA increased whereas MLT decreased, but such hormone has no effect on coincubation. DHA isolated did not change the oxidative phosphorylation rate (OXPHOS), but decreased (p < 0.001) the mitochondria' bioenergetic reserve capacity (MBRC) which is closely related to cell responsiveness to stress conditions. MLT, regardless of DHA, ameliorated OXPHOS and recovered MBRC after coincubation. All incubations decreased AKT phosphorylation; however, only MLT alone inhibited p-mTOR. MLT increased p-ERK1/2 and, when combined to DHA, increased GSTP1 expression (p < 0.01). DHA did not change the testosterone levels in the medium, whereas MLT alone or coincubated decreased by about 20%; however, any incubation affected AR expression. Moreover, incubation with luzindole revealed that MLT effects were MTR1/2-independent. In conclusion, DHA increased ROS production and impaired mitochondrial function which was probably related to AKT inactivation; MLT improved OXPHOS and decreased ROS which was related to AKT/mTOR dephosphorylation, and when coincubated, the antiproliferative action was related to mitochondrial bioenergetic modulation associated to AKT and ERK1/2 regulation. Together, these findings point to the potential application of DHA and MLT towards the prevention of proliferative prostate diseasespt_BR
dc.relation.ispartofOxidative medicine and cellular longevitypt_BR
dc.relation.ispartofabbreviationOxid. med. cell. longev.pt_BR
dc.publisher.cityLondonpt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherHindawipt_BR
dc.date.issued2019-
dc.date.monthofcirculationJan.pt_BR
dc.language.isoengpt_BR
dc.description.volume219pt_BR
dc.rightsAbertopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1942-0900pt_BR
dc.identifier.eissn1942-0994pt_BR
dc.identifier.doi10.1155/2019/5080798pt_BR
dc.identifier.urlhttps://www.hindawi.com/journals/omcl/2019/5080798/pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumber308367/2014-6; 309764/2015-7pt_BR
dc.description.sponsordocumentnumbernão tempt_BR
dc.description.sponsordocumentnumber2018/19590-6; 2015/13371-2; 2015/24595-9; 2013/16368-7pt_BR
dc.description.sponsordocumentnumber002/2018pt_BR
dc.date.available2020-06-05T12:59:48Z-
dc.date.accessioned2020-06-05T12:59:48Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-06-05T12:59:48Z No. of bitstreams: 0. Added 1 bitstream(s) on 2020-09-03T11:55:47Z : No. of bitstreams: 1 000456643600001.pdf: 5669939 bytes, checksum: fdef7117ee4432412d3320a7de1c851f (MD5)en
dc.description.provenanceMade available in DSpace on 2020-06-05T12:59:48Z (GMT). No. of bitstreams: 0 Previous issue date: 2019en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/342739-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Bioquímica e Biologia Tecidualpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source000456643600001pt_BR
dc.creator.orcid0000-0001-6584-6566pt_BR
dc.creator.orcid0000-0002-1075-8830pt_BR
dc.type.formArtigo de pesquisapt_BR
dc.identifier.articleid5080798pt_BR
dc.description.otherSponsorshipFundação dePesquisa e Extensão de São José do Rio Preto - FAPERPpt_BR
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