Person: ATASOY, BESTE MELEK
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ATASOY
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BESTE MELEK
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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 Radiation-induced oxidative injury of the ileum and colon is alleviated by glucagon-like peptide-1 and -2(ELSEVIER SCIENCE BV, 2015-04) ATASOY, BESTE MELEK; Deniz, Mustafa; Atasoy, Beste M.; Dane, Faysal; Can, Guray; Erzik, Can; Cetinel, Sule; Yegen, Berrak C.Purpose: The present study was conducted to characterize the possible therapeutic effects of glucagon-like peptide (GLP)-1 and GLP-2 against oxidative damage in the ileum and colon of irradiated rats. Methods and materials: Sprague-Dawley rats of both sexes received either a single dose of GLP-1 (0.1 nmol/kg, intraperitoneally, ip; n = 6) 10 min before abdominal irradiation (IR) or two consecutive doses of GLP-2 (7 nmol/kg, ip; n = 6) at 30 and 10 min before IR, while another group was administered vehicle (n = 6) 10 min before IR. Control rats (n = 6) received vehicle treatment without IR. On the fourth day of IR, samples from ileum and colon were removed for histological analysis, for the determination of myeloperoxidase (MPO) activity, malondialdehyde (MDA) and glutathione (GSH) levels, as well as DNA fragmentation ratio, an index of apoptosis. Results: IR-induced oxidative injury in the colonic tissue of vehicle-treated rats, evidenced by elevated MDA levels and MPO activity, as well as depleted colonic GSH levels, was reversed by GLP-2, while GLP-1 reduced IR-induced elevations in colonic MDA levels. IR-induced injury with elevated ileal MDA levels was reduced by GLP-1, while replenishment in GSH was observed in GLP-2-treated rats. Conclusion: Current findings suggest that GLP-1 and GLP-2 appear to have protective roles in the irradiation-induced oxidative damage of the gut by inhibiting neutrophil infiltration and subsequent activation of inflammatory mediators that induce lipid peroxidation. Copyright (C) 2015, The Egyptian Society of Radiation Sciences and Applications. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license.