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    The influencer effect of Dexmedetomidine on radioiodine relevant to lacrimal gland impairment
    (Springer, 2024) Singar, Evin; Akbulut, Aylin; Koca, Goekhan; Yazihan, Nuray; Atilgan, Hasan Ikbal; Yumusak, Nihat; Demir, Ayten
    PurposeTo assess the potential influencing effects of Dexmedetomidine on impaired lacrimal glands after high-dose radioiodine treatment (RAI). MethodsThirty-six rats were arbitrarily separated into 3 groups: Sham, RAI, and Dexmedetomidine. Dexmedetomidine group was given Dexmedetomidine and RAI, the Sham group was given the same millimeters of saline, and the RAI group was given RAI only. All forms of lacrimal glands, including harderian glands (HG), extraorbital (EG), and intraorbital (IG) lacrimal glands, were evaluated for immunohistochemical, histopathologic assessments and also for tissue cytokines, oxidant and antioxidant levels. ResultsDexmedetomidine significantly ameliorated histopathologic changes such as periacinar fibrosis, acinar atrophy, lymphocytic infiltration, ductal proliferation, lipofuscin-like accumulation, and nucleus changes caused by RAI in all lacrimal gland forms (p < 0.05 for all of the parameters). However, periductal fibrosis was improved significantly only in EG (p = 0.049), and mast cell infiltration was improved significantly only in IG (p = 0.038) in Dexmedetomidine groups. There was a significant decrease in the elevated caspase-3 and TUNEL levels after RAI administration in the Dexmedetomidine group in all lacrimal gland forms (p < 0.05 for all parameters). Dexmedetomidine attenuated NF-kb, TNF-alpha, and IL-6 levels significantly diminished total oxidant status and raised total antioxidant status levels (p < 0.05 for all parameters). ConclusionsThe results of this study demonstrated that following RAI, Dexmedetomidine diminished inflammation, tissue cytokine levels, and apoptosis and ameliorated impaired histopathologic patterns of the lacrimal glands.
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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.