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    Evaluation of the protective effects of hesperetin against cisplatin-induced ototoxicity in a rat animal model
    (Elsevier Ireland Ltd, 2016) Kara, Medine; Turkon, Hakan; Karaca, Turan; Guclu, Oguz; Uysal, Sema; Turkyilmaz, Mehmet; Demirtas, Selim
    Objectives: We aimed to investigate the effects of hesperetin as a flavanon both histopathologically and immunohistochemically on cochlear apoptosis in a rat model of cisplatin-induced ototoxicity (CIO). The evaluation of the effects of hesperetin on cisplatin-induced hearing loss was performed using distortion product otoacoustic emission (DPOAE). Methods: Twenty-eight wistar albino rats were used in the current study. The rats were randomly divided into four groups with seven rats in each group. Group C was exposed to a single dose of cisplatin (12 mg/kg) by intraperitoneal injection. Group CH received intraperitoneally cisplatin (12 mg/kg) and hesperetin (20 mg/kg). Group H was exposed to hesperetin (20 mg/kg) intraperitoneally. The sham group (group S) received normal saline (6 cc) intraperitoneally. The measurements of DPOAE and signal-noise ratios (SNR) were performed before the treatment and again on the first and 6 days after administration of the drugs. Rats were sacrificed and cochleae were dissected 10 days after drug administration. The cochlear tissue was assessed in all groups by histopathologic, immunohistochemical and TUNEL assay. In addition, serum oxidative stress markers and antioxidant parameters were analyzed. Results: There was a significant difference between the basal value and the sixth day at frequencies 8.4, 9.6 and 9.96 for group C. We also found a significant difference between the first and sixth day at frequencies 7.2, 8.4, 9.6 and 9.96. On the 6th day, there were significant differences between C and S groups at all frequencies except 2.4. We showed a significant difference between C and H groups at frequencies 4.8, 6.0, 8.4, 9.6 and 9.96. There was also a significant difference between C and CH groups at frequencies 2.4, and 3.6. We found lower levels of oxidants and higher levels of antioxidants in CH group as compared to C group. C group had a significantly greater number of TUNEL-positive cells than did S, H and CH groups. The number of TUNEL-positive cells in CH group was higher than in S and H groups. There was a significant difference between the positive PCNA cells of CH group compared to S and H groups in spiral ganglion and stria vascularis. In addition, there were no positive PCNA cells in C group. Conclusions: Hesperetin may prevent ototoxicity by increased antioxidant enzymes and reduced oxidant parameters and protected against apoptosis resulting from a proliferation of cochlear cells in CIO. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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    The protective effect of quercetin on IMA levels and apoptosis in experimental ovarian ischemia-reperfusion injury
    (Elsevier Science Bv, 2014) Gencer, Meryem; Karaca, Turan; Gungor, Ayse N. C.; Hacivehoglu, Servet O.; Demirtas, Selim; Turkon, Hakan; Uysal, Ahmet
    Objective: To investigate the protective effect of quercetin (QE), an anti-inflammatory and anti-oxidant agent, on torsion-detorsion induced histopathological changes and blood IMA levels in experimental ovarian ischemia-reperfusion (IR) injury. Study design: Twenty-four female Wistar rats were randomly divided into four groups in this study (n = 6). Group I, (sham operation); Group II, torsion-detorsion plus saline (IR); Group III, torsiondetorsion plus solvent (dimethylsulfoxide: DMSO, IR + DMSO); Group IV, torsion-detorsion plus 15 mg/kg/bw quercetin (IR + QE) injected intraperitoneally 30 min prior to detorsion. After 3 h of reperfusion, the right ovaries were removed surgically. The ovary tissue samples were fixed in 10% formalin solution for histopathological and immunohistochemical examination. Blood samples were obtained at the end of the procedures for each group of animals. Results: Ovarian sections in Groups II and III showed higher follicular cell degeneration, hemorrhage, vascular congestion and edema when compared with Group I. Administration of quercetin in rats significantly prevented degenerative changes in the ovary. Significantly less histopathological changes were found in Group IV compared with Groups II and III. Caspase-3 and TUNEL positive cells were detected in the ovarian surface, follicle epithelium, and stromal cells in all experimental groups, and there was a significant increase in Groups II and III compared with Group I (P < 0.05). Treatment with quercetin decreased the number of caspase-3 and TUNEL positive cells. IR increased the ischemia modified albumin (IMA) levels in comparison to the sham group (1.06 +/- 0.10 ABSU and 0.92 +/- 0.08 ABSU, P < 0.05). Quercetin administration before IR reduced the levels of IMA (0.93 + 0.08 ABSU, P < 0.05). Conclusion: Administration of quercetin is effective in preventing tissue damage induced by IR injury in ovaries. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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    The Role of Melatonin in Oxidative Stress, DNA Damage, Apoptosis and Angiogenesis in Fetal Eye under Preeclampsia and Melatonin Deficiency Stress
    (Taylor & Francis Inc, 2019) Doganlar, Zeynep Banu; Guclu, Hande; Oztopuz, Ozlem; Turkon, Hakan; Dogan, Ayten; Uzun, Metehan; Doganlar, Oguzhan
    Aim: The aim of this study was to investigate the possible mechanisms of ocular damage induced by pinealectomy (PNX) and preeclampsia (PE), and to determine the cellular and molecular effects of melatonin treatment on oxidative stress, DNA damage, molecular chaperone responses, induction of apoptosis and angiogenesis in the fetal eye of both PNX and PNX+PE animals. Material and Methods: We analysed therapeutic potential of melatonin on fetal eye damage in PNX and PNX+PE animals using Malondialdehyde (MDA), Random Amplified Polymorphic DNA (RAPD), qRT-PCR and Western blot assays. Results: Our study presents three preliminary findings: (a) in fetal eye tissues, PNX and PNX+PE significantly induce oxidative damage to both DNA and protein contents, leading to a dramatic increase in caspase-dependent apoptotic signalling in both mitochondrial and death receptor pathways; (b) the same conditions trigger hypoxia biomarkers in addition to significant overexpression of HIF1-alpha, HIF1-beta, MMP9 and VEGF genes in the fetal eye; (c) finally, melatonin regulates not only the expression of genes encoding antioxidant enzymes and increase in DNA damage as well as lipid peroxidation but also limits programmed cell death processes in the fetal eye of PNX and PNX+PE animals . Furthermore, melatonin can relatively modulate genes in the HIF1 family, TNF-alpha and VEGF, thus acting as a direct anti-angiogenic molecule. In conclusion, both PNX and PNX+PE induce ocular damage at both cellular and molecular levels in fetal eye tissue of rats. Conclusion: Our results clearly indicate the potential of melatonin as a preventative therapeutic intervention for fetal ocular damage triggered by both PNX and PNX+PE.