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dc.contributor.authorErkan, Melike
dc.contributor.authorYildizbayrak, Nebahat
dc.date.accessioned2021-03-05T21:57:28Z
dc.date.available2021-03-05T21:57:28Z
dc.date.issued2018
dc.identifier.citationYildizbayrak N., Erkan M., "Acrylamide disrupts the steroidogenic pathway in Leydig cells: possible mechanism of action", TOXICOLOGICAL AND ENVIRONMENTAL CHEMISTRY, cilt.100, ss.235-246, 2018
dc.identifier.issn0277-2248
dc.identifier.othervv_1032021
dc.identifier.otherav_db5b11d4-cdad-4f5c-8ca6-285f9adcf7cc
dc.identifier.urihttp://hdl.handle.net/20.500.12627/144597
dc.identifier.urihttps://doi.org/10.1080/02772248.2018.1458231
dc.description.abstractAcrylamide-treated Leydig cells were tested for cytotoxicity, testosterone secretion, 3,5-cyclic adenosine monophosphate production, and gene and protein expression of steroidogenic genes and transcription factors. Reverse-transcriptional real-time polymerase chain reaction and western blot analysis revealed that acrylamide disrupts mRNA and protein expression of steroidogenic markers, including luteinizing hormone receptor, steroidogenic acute regulatory protein, cholesterol side-chain cleavage enzyme, 3-hydroxy dehydrogenase, and 17-hydroxy dehydrogenase. Further, transcription levels of the key regulator transcription factors, steroidogenic factor-1, GATA binding protein-4, and nerve growth factor IB, were evaluated. Acrylamide induced cytotoxicity and decreased testosterone and 3,5-cyclic adenosine monophosphate secretion by altering the rate-limiting steps in Leydig cell steroidogenesis.
dc.language.isoeng
dc.subjectFarmakoloji ve Toksikoloji
dc.subjectMühendislik ve Teknoloji
dc.subjectTemel Bilimler
dc.subjectTOKSİKOLOJİ
dc.subjectYaşam Bilimleri
dc.subjectÇevre Mühendisliği
dc.subjectÇEVRE BİLİMLERİ
dc.subjectÇevre / Ekoloji
dc.subjectTarım ve Çevre Bilimleri (AGE)
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectSağlık Bilimleri
dc.subjectEczacılık
dc.subjectTarımsal Bilimler
dc.subjectMeslek Bilimleri
dc.subjectFarmasötik Toksikoloji
dc.titleAcrylamide disrupts the steroidogenic pathway in Leydig cells: possible mechanism of action
dc.typeMakale
dc.relation.journalTOXICOLOGICAL AND ENVIRONMENTAL CHEMISTRY
dc.contributor.department, ,
dc.identifier.volume100
dc.identifier.issue2
dc.identifier.startpage235
dc.identifier.endpage246
dc.contributor.firstauthorID248653


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