Person: ŞENER, GÖKSEL
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ŞENER
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GÖKSEL
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Publication Open Access Classification and Premedication of Uncooperative Children.(1993) ŞENER, GÖKSEL; Simsek, S.; Akyüz, S.; Sener, G.; Göker, K.; Güvener, Ö.Publication Open Access Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats(BIOSCIENTIFICA LTD, 2006-05) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G.; Kabasakal, L.; Atasoy, B. M.; Erzik, C.; Velioglu-Ogunc, A.; Cetinel, S.; Contuk, G.; Gedik, N.; Yegen, B. C.The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and turnout necrosis factor-alpha (TNF alpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P < 0.05-0.001). Similarly, serum TNFa and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.Publication Open Access Melatonin protects against acrylamideinduced oxidative tissue damage in rats(2012-01-01) BECEREN, AYFERPublication Open Access Effects of Exercise and Calorie Restriction on Brain_x000D_ and Testis in Natural Aging Model(2021-04-25) YARAT, AYŞEN; Umay HAKGÜDER;Hazal İPEKÇİ;Tuğba TUNALI AKBAY;Ayşen YARAT;Ebru Emekli ALTURFAN;Ünsal Veli ÜSTÜNDAĞ;Burçin ALEV;Nevin GENC KAHRAMAN;Reyhan ÖZÇELİK;Göksel ŞENERThe aim of our study was to examine the effects of exercise and calorie_x000D_ restriction on various tissue damage and antioxidant parameters_x000D_ in the brain and testis of rats in a natural aging model. For this_x000D_ purpose, male Sprague-Dawley rats were the control group (C),_x000D_ the elderly (A), the elderly with calorie restriction (ACR), the elderly_x000D_ who were exercised (AE) and the elderly who were exercised with_x000D_ calorie restriction (ACRE), they were divided into 5 groups. The control_x000D_ group was composed of three-month-old animals. The other_x000D_ group consisted of 15-month-old rats. Exercise and calorie restriction_x000D_ were applied for 6 weeks. At the end of the experiment, lipid_x000D_ peroxidation (LPO), nitric oxide (NO), glutathione (GSH) levels and_x000D_ superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase_x000D_ (GST) and tissue factor (TF) were determined in brain and_x000D_ testicular tissues homogenates. As a result of the study, the A_x000D_ group’s brain and testis LPO, NO levels and TF activity increased,_x000D_ GSH levels and SOD, CAT and GST activities decreased, when compared_x000D_ to the C group. As a result of our study, an increase in oxidant_x000D_ damage was observed with TF activity in the brain and testis in the_x000D_ natural aging model, and positive effects of exercise and calorie_x000D_ restriction on the antioxidant levels in the brain were determined,_x000D_ especially in aging.Publication Open Access Protective effects of quercetin against cisplatin induced urogenital organ toxicity(MARMARA UNIV, 2020-09-11) ERCAN, FERİHA; Sener, Tarik Emre; Cadirci, Selin; Cevik, Ozge; Ercan, Feriha; Koroglu, M. Kutay; Sakarcan, Selin; Sener, GokselCisplatin is a chemotherapeutic agent that is the first to enter treatment from organic platinum-derived drugs. Nephrotoxicity and cytotoxicity are major factors that limit its use. The aim of the study is to investigate the possible protective effects of quercetin against cisplatin-induced urogenital organ toxicity. In our study, Sprague Dawley four month old male rats were divided into 4 groups; control + saline (SF), control + quercetin (20 mg/kg for 21 days), cisplatin (7 mg/kg as a single dose) + SF and cisplatin + quercetin groups. After decapitation, the kidney, bladder, testis and corpus cavernosum tissue samples were taken to analyze caspase-3, an index of apoptosis, and oxidative stress parameters such as malondialdehyde (MDA), gluta-thione (GSH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Furthermore, tissues were also examined histologically. Cisplatin caused significant increases in MDA and 8-OHdG levels, demonstrating increases in lipid peroxidation and oxidative DNA damage, respectively, in all tissues. In parallel with the oxidant stress increase, the endogenous strong antioxidant GSH levels were decreased. Caspase activity and caspase 3 expressions, which we measured as an indicator of apoptosis, increased significantly with cisplatin treatment. On the other hand, treatment with quercetin, a powerful antioxidant flavonoid, reversed these changes. Histological findings also demonstrated well-preserved tissues due to quercetin treatment. In conclusion, our results suggested that quercetin, when given with cisplatin, can be protective against the chemotherapeutic induced toxicity and thus provide therapeutic benefit.Publication Open Access Protective effects ofGinkgo biloba extract against mercury(II)-induced cardiovascular oxidative damage in rats(2007-01) YARAT, AYŞEN; Tunali-Akbay, Tugba; Sener, Goksel; Salvarli, Hanife; Sehirli, Ozer; Yarat, AysenPublication Open Access Tadalafil attenuates spinal cord injury induced oxidative organ damage in rats(2014-05-13) ŞENER, GÖKSELPublication Open Access Exercise and caloric restriction improve cardiovascular and erectile function in rats with metabolic syndrome(2020-12-01) ŞENER, TARIK EMRE; ŞENER, GÖKSEL; Çevikelli Yakut Z. A., Özçelik R., Çevik Ö., Şener T. E., Şener G.The aim of this study is to examine the possible benefits of exercise and caloric restriction (CR) on cardiovascular hemodynamics, erectile function, and antioxidant system in metabolic syndrome (MS). Sixty male Spraque-Dawley rats were divided into five groups; control, MS, MS + CR, MS + exercise (EXC), and MS + CR + EXC. To induce MS, 10% fructose solution was applied for 3 months. Thereafter, in CR groups calorie was restricted 40% and in EXC groups swimming was performed for 6 weeks. Body weight, blood glucose, and blood pressure (BP) levels were measured before and after MS induction and at the end of the experiment. After decapitation, tumor necrosis factor (TNF)-α, adiponectin (ADP), and plasminogen activator inhibitor (PAI)-1 levels were investigated in blood, oxidative stress parameters were examined in heart, aorta, and corpus cavernosum (CC) tissues. Isometric contraction in isolated tissue bath was studied in aorta and CC tissues. Animals subjected to exercise and CR had decreased BP and blood glucose levels. Impaired contraction-relaxation responses in MS group were improved with exercise and CR. MS-induced increase in TNF-α, PAI-1, malondialdehyde (MDA), and decrease in ADP, glutathione (GSH), and superoxide dismutase (SOD) were normalized with exercise and CR. Exercise and CR may be beneficial against changes in cardiovascular hemodynamics caused by MS.Publication Open Access Melatonin protects against mercury(II)-induced oxidative tissue damage in rats(BLACKWELL MUNKSGAARD, 2003-12) ŞENER, GÖKSEL; Sener, G; Sehirli, AO; Ayanoglu-Dulger, GMercury exerts a variety of toxic effects in the body. Lipid peroxidation, DNA damage and depletion of reduced glutathione by Hg(II) suggest an oxidative stress-like mechanism for Hg(II) toxicity. Melatonin, the main secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. N-Acetylcysteine, a precursor of reduced glutathione and an antioxidant, is used in the therapy of acute heavy metal poisoning. In this study the protective effects of melatonin in comparison to that of N-acetylcysteine against Hg-induced oxidative damage in the kidney, liver, lung and brain tissues were investigated. Wistar albino rats of either sex (200-250 g) were divided into six groups, each consisting of 8 animals. Rats were intraperitoneally injected with 1) 0.9% NaCl, control (C) group; 2) a single dose of 5 mg/kg mercuric chloride (HgCl2), Hg group; 3) melatonin in a dose of 10 mg/kg, I hr after HgCl2 injection, Hg-melatonin group; 4) melatonin in a dose of 10 mg/kg one day before and 1 hr after HgCl2 injection, melatonin-Hg-melatonin group; 5) N-acetylcysteine in a dose of 150 mg/kg, I hr after HgCl2 injection, Hg-N-acetylcysteine group, and 6) N-acetylcysteine in a dose of 150 mg/kg one day before and I hr after HgCl2 injection, N-acetylcysteine-Hg-N-acetylcysteine group. Animals were killed by decapitation 24 hr after the injection of HgCl2. Tissue samples were taken for determination of malondialdehyde, an end-product of lipid peroxidation; glutathione (GSH), a key antioxidant, and myeloperoxidase activity, an index of neutrophil infiltration. The results revealed that HgCl2 induced oxidative tissue damage, as evidenced by increases in malondialdehyde levels. Myeloperoxidase activity was also increased, and GSH levels were decreased in the liver, kidney and the lungs. All of these effects were reversed by melatonin or N-acetylcysteine treatment. Since melatonin or N-acetylcysteine administration reversed these responses, it seems likely that melatonin or N-acetylcysteine can protect all these tissues against HgCl2-induced oxidative damage.Publication Open Access