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dc.contributor.authorAydemir, Duygu
dc.contributor.authorKarabulut, Gözde
dc.contributor.authorGok, Muslum
dc.contributor.authorBarlas, Nurhayat
dc.contributor.authorUlusu, Nuriye Nuray
dc.date.accessioned2021-06-03T09:00:41Z
dc.date.available2021-06-03T09:00:41Z
dc.date.issued2019
dc.identifier.issn2352-3409
dc.identifier.urihttp://dx.doi.org/10.1016/j.dib.2019.104526
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6811911/
dc.identifier.urihttp://hdl.handle.net/11655/24384
dc.description.abstractDi (2-ethylhexyl) phthalate (DEHP) is used as plasticizer in the industry and belongs to the phthalate family which can induce tissue damage including kidney, liver, and testis as a result of elevated oxidative stress levels. Glutathione reductase (GR), Glucose-6-phosphate dehydrogenase (G6PD), glutathione S-transferase (GST), 6-phosphogluconate dehydrogenase (6PGD), enzyme activities, trace element and mineral levels were evaluated in the brain and testis tissue samples. Our data revealed that, antioxidant enzyme activities in the brain and testis samples were statistically insignificant in the DEHP administered groups compared to the control group except 400 mg/kg/day DEHP dose group in the testis samples. DEHP can disrupt trace element and mineral levels unlike antioxidant enzyme levels that may due to blood-brain and testis-blood barrier and/or short-term exposure to the DEHP. For more detailed information than the data presented in this article, please see the research article “Impact of the Di (2-Ethylhexyl) Phthalate Administration on Trace Element and Mineral Levels in Relation of Kidney and Liver Damage in Rats” [1].
dc.language.isoen
dc.relation.isversionof10.1016/j.dib.2019.104526
dc.rightsAttribution 4.0 United States
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleData The Dehp Induced Changes On The Trace Element And Mineral Levels In The Brain And Testis Tissues Of Rats
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalData In Brief
dc.contributor.departmentBiyokimya
dc.identifier.volume26
dc.description.indexPubMed
dc.description.indexWoS
dc.description.indexScopus


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Attribution 4.0 United States
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