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  • Küçük Resim
    Öğe
    Apoptosis and cell proliferation in short-term and long-term effects of radioiodine-131-induced kidney damage: an experimental and immunohistochemical study
    (Lippincott Williams & Wilkins, 2018) Yumusak, Nihat; Sadic, Murat; Yucel, Gozde; Atilgan, Hasan I.; Koca, Gokhan; Korkmaz, Meliha
    ObjectiveRadioiodine-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.
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    Proliferative and apoptotic evaluations of renal preventive effects of coenzyme Q10 in radioiodine-131 induced renal damage
    (Ankara Univ Press, 2022) Yumusak, Nihat; Koca, Gokhan; Akbulut, Aylin; Atilgan, Hasan Ikbal; Korkmaz, Meliha
    The aim of this study was to investigated anti-proliferative and anti-apoptotic effects of coenzyme Q10 (CoQ10) in the prevention of radioiodine-131 (RAI) (I-1(31)) induced kidney damage. A total of 24 Wistar albino rats were separated into equal three groups (n = 8/group): Group 1 (control): untreated group; Group 2 (RAI): 3 mCi/kg RAI oral route; Group 3 (RAI+CoQ10): 3 mCi/kg RAI oral route and intraperitoneally 30 mg/kg/day CoQ10. CoQ10 treatment was started two days before RAI administration and was continued five days once daily after RAI. Pathomorphological parameters of kidneys were measured using hematoxylin-eosin and Masson's trichrome staining. Immunohistochemically; proliferating cell nuclear antigen (PCNA), caspase 8, caspase 9 and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) were used to determine proliferation and apoptosis. With the exception of the control group, varying degrees of inflammation, degeneration, necrosis, and interstitial/perivascular fibrosis were detected in the kidneys of all rats. This histopathological damage was found to be significantly less in CoQ10 group versus RAI group (P<0.05). The all immunohistochemical examinations demonstrated that administration of CoQ10 had reduced proliferation and apoptosis (P<0.05). The results of kidney histopathology and immunohistochemistry demonstrated that administration of CoQ10 had reduced inflammation, proliferation, and apoptosis. These fmdings show CoQ10 can play an important role in the radioprotection of kidneys against RAI-induced damage.