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Acrylamide and Its Metabolite Glycidamide Induce Reproductive Toxicity During In Vitro Maturation of Bovine Oocytes

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dc.contributor.authorEl-Sheikh, Marwa-
dc.contributor.authorMesalam, Ahmed Atef-
dc.contributor.authorMesalam, Ayman-
dc.contributor.authorKong, Il-Keun-
dc.date.accessioned2025-05-02T07:30:16Z-
dc.date.available2025-05-02T07:30:16Z-
dc.date.issued2025-03-
dc.identifier.issn2305-6304-
dc.identifier.issn2305-6304-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/77963-
dc.description.abstractAcrylamide (ACR) and its metabolite glycidamide (GLY) are contaminants with known toxic effects, especially in reproductive systems. However, the mechanisms underlying their embryotoxic effects remain inadequately understood. In the current study, we investigated the effects of ACR and GLY exposure on oocyte and embryo developmental competence, focusing on DNA damage, apoptosis, autophagy, and epigenetic regulation. Oocytes were exposed to varying concentrations of ACR and GLY during in vitro maturation. The results demonstrated that both ACR and GLY significantly reduced cleavage and blastocyst developmental rates in a dose-dependent manner. Consequently, treated oocytes exhibited actin organization disruption, increased DNA damage, and heightened apoptosis compared to the control. Autophagy-related markers, including LC3A, LC3B, and ATG7, were significantly elevated in the treatment groups. Moreover, both ACR and GLY compounds altered the expression of the epigenetic and MAPK signaling pathway regulators, such as DPPA3, EZH1, EZH2, EED, DUSP1, and ASK1. These disruptions collectively impaired embryonic development. This study underscores the adverse effects of ACR and GLY on reproductive health, driven by oxidative stress, genotoxicity, dysregulated autophagy, and epigenetic alterations.-
dc.language영어-
dc.language.isoENG-
dc.publisherMDPI AG-
dc.titleAcrylamide and Its Metabolite Glycidamide Induce Reproductive Toxicity During In Vitro Maturation of Bovine Oocytes-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.3390/toxics13030223-
dc.identifier.scopusid2-s2.0-105002056592-
dc.identifier.wosid001453324900001-
dc.identifier.bibliographicCitationToxics, v.13, no.3-
dc.citation.titleToxics-
dc.citation.volume13-
dc.citation.number3-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEnvironmental Sciences & Ecology-
dc.relation.journalResearchAreaToxicology-
dc.relation.journalWebOfScienceCategoryEnvironmental Sciences-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.subject.keywordPlusENVIRONMENTAL DEGRADATION-
dc.subject.keywordPlusDNA METHYLATION-
dc.subject.keywordPlusPOLYACRYLAMIDES-
dc.subject.keywordPlusNEUROTOXICITY-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusFERTILITY-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusEVENTS-
dc.subject.keywordPlusCELLS-
dc.subject.keywordAuthoracrylamide-
dc.subject.keywordAuthorglycidamide-
dc.subject.keywordAuthoroocyte-
dc.subject.keywordAuthorautophagy-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorepigenetics-
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