Apoptosis and cell proliferation in short-term and long-term effects of radioiodine-131-induced kidney damage: an experimental and immunohistochemical study

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dc.authoridYucel Tenekeci, Gozde/0000-0002-2586-8346
dc.contributor.authorYumusak, Nihat
dc.contributor.authorSadic, Murat
dc.contributor.authorYucel, Gozde
dc.contributor.authorAtilgan, Hasan I.
dc.contributor.authorKoca, Gokhan
dc.contributor.authorKorkmaz, Meliha
dc.date.accessioned2024-09-18T20:02:34Z
dc.date.available2024-09-18T20:02:34Z
dc.date.issued2018
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractObjectiveRadioiodine-131 is a radionuclide that is used for therapeutic purposes in hyperthyroidism and thyroid cancer. The aim of this study was to evaluate apoptotosis and proliferative changes in radioiodine-related kidney damage.Materials and methodsThree groups (n=10/group) of rats were used as follows: the rats were in group 1 untreated, and the rats in groups 2 and 3 were treated once with oral radioiodine (111MBq). The animals in group 2 were killed at the end of the seventh day and the rats in group 3 were killed at the end of the 10th week. The kidneys were removed and evaluated immunohistochemically. The presence of radioiodine in the kidneys was shown by the Na+/I-symporter antibody and proliferating cell nuclear antigen, Ki-67, caspase-3, caspase-8, caspase-9, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling assay were used to detect cell proliferation and apoptosis.ResultsNa+/I-symporter protein accumulation in the kidneys was observed to be significantly greater in group 2 than in group 3 (P<0.05). All the immunohistochemical analyses showed that cell proliferation and apoptosis began on the seventh day and peaked in the 10th week. The proliferating cell nuclear antigen, Ki-67, and caspase expressions and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling values were all found to be statistically significantly increased in group 3 compared with the other groups (P<0.05).ConclusionRadioiodine caused cell proliferation and apoptosis as shown by immunohistochemistry.en_US
dc.identifier.doi10.1097/MNM.0000000000000788
dc.identifier.endpage139en_US
dc.identifier.issn0143-3636
dc.identifier.issn1473-5628
dc.identifier.issue2en_US
dc.identifier.pmid29257007en_US
dc.identifier.scopus2-s2.0-85043487972en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage131en_US
dc.identifier.urihttps://doi.org/10.1097/MNM.0000000000000788
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7871
dc.identifier.volume39en_US
dc.identifier.wosWOS:000427034900006en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.ispartofNuclear Medicine Communicationsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectapoptosisen_US
dc.subjectcell proliferationen_US
dc.subjectkidneyen_US
dc.subjectradiationen_US
dc.subjectradioiodineen_US
dc.titleApoptosis and cell proliferation in short-term and long-term effects of radioiodine-131-induced kidney damage: an experimental and immunohistochemical studyen_US
dc.typeArticleen_US

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