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BECEREN, AYFER

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2007 - 200912010 - 20122
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Author: ŞENER, GÖKSEL × Subject: CELLS ×

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Now showing 1 - 3 of 3
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    Ginkgo biloba extract reduces naphthalene-induced oxidative damage in mice
    (JOHN WILEY & SONS LTD, 2007-01) BECEREN, AYFER; Tozan, Ayfer; Sehirli, Ozer; Omurtag, Gulden Z.; Cetinel, Sule; Gedik, Nursal; Sener, Goksel
    This investigation elucidated the role of free radicals in naphthalene-induced toxicity and protection by Ginkgo biloba extract (EGb). BALB-c mice of either sex were administered with naphthalene (100 mg/kg; i.p.) for 30 days, along with either saline or EGb (150 mg/kg, orally). At the end of the experiment, following decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. In addition, proinflammatory cytokines (TNF-alpha and IL-beta) and total antioxidant capacity (AOC) were assayed in the plasma, while lactate dehydrogenase (LDH) activity was assayed in serum samples. The results revealed that naphthalene caused a significant decrease in GSH level, and significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, plasma cytokines, as well as serum LDH activity, were elevated while AOC was decreased in the naphthalene group compared with the control group. On the other hand, EGb treatment reversed all these biochemical indices. The results demonstrate that EGb extract, by balancing the oxidant-antioxidant status and inhibiting the generation of proinflammatory cytokines and neutrophil infiltration, protects against naphthalene-induced oxidative organ injury. Copyright (c) 2006 John Wiley & Sons, Ltd.
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    Resveratrol ameliorates oxidative DNA damage and protects against acrylamide-induced oxidative stress in rats
    (SPRINGER, 2012) BECEREN, AYFER; Alturfan, A. Ata; Tozan-Beceren, Ayfer; Sehrili, Ahmet Ozer; Demiralp, Emel; Sener, Goksel; Omurtag, Gulden Zehra
    Acrylamide (ACR), used in many fields from industrial manufacturing to laboratory personnel work is also formed during the heating process through interactions of amino acids. Therefore ACR poses a significant risk to human health. This study aimed to elucidate whether resveratrol (RVT) treatment could modulate ACR-induced oxidative DNA damage and oxidative changes in rat brain, lung, liver, kidney and testes tissues. Rats were divided into four groups as control (C); RVT (30 mg/kg i.p. dissolved in 0.9% NaCl), ACR (40 mg/kg i.p.) and RVT + ACR groups. After 10 days rats were decapitated and tissues were excised. 8-hydroxydeoxyguanosine (8-OHdG) is a biomarker of oxidative DNA damage. 8-OHdG content in the extracted DNA solution was determined by enzyme-linked immunosorbent assay method. Malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase activity (MPO) were determined in tissues, while oxidant-induced tissue fibrosis was determined by collagen contents. Serum enzyme activities, cytokine levels, leukocyte apoptosis were assayed in plasma. As an indicator of oxidative DNA damage, 8-OHdG levels significantly increased in ACR group and this was reversed significantly by RVT treatment. In ACR group, GSH levels decreased significantly while the MDA levels, MPO activity and collagen content increased in the tissues suggesting oxidative organ damage. In RVT-treated ACR group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels and leukocyte late apoptosis which increased following ACR administration, decreased with RVT treatment. Therefore supplementing with RVT can be useful in individuals at risk of ACR toxicity.
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    Protective effect of N-acetyl-L-cysteine against acrylamide-induced oxidative stress in rats
    (SCIENTIFIC TECHNICAL RESEARCH COUNCIL TURKEY-TUBITAK, 2012) BECEREN, AYFER; Alturfan, Ebru Isik; Beceren, Ayfer; Sehirli, Ahmet Ozer; Demiralp, Zeynep Emel; Sener, Goksel; Omurtag, Gulden Zehra
    Acrylamide (AA), used in many fields, from industrial manufacturing to laboratory work, is also formed during the heating process through the interactions of amino acids. Therefore, AA poses a significant risk for both human and animal health. This study aimed to elucidate whether N-acetyl-L-cysteine (NAC) treatment could modulate AA-induced oxidative changes in the brain, lung, liver, kidney, and testes tissues of the rat. Rats were divided into 4 groups, as the control (C), NAC [150 mg/kg intraperitoneally (i.p.)], AA (40 mg/kg i.p.), and NAC + AA groups. After 10 days, the rats were decapitated and the tissues were excised. Malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase activity (MPO) were determined in the tissues, while oxidant-induced tissue fibrosis was determined using the collagen contents. Serum enzyme activities, cytokine levels, and leukocyte apoptosis were assayed in the plasma. In the AA group, GSH levels decreased significantly, while the MDA levels, MPO activity, and collagen content increased in the tissues suggesting oxidative organ damage. In the NAC + AA group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels, and leukocyte apoptosis, which increased following AA administration, decreased with NAC treatment. Therefore, supplementing with NAC can be useful when there is a risk of AA toxicity, as NAC inhibits neutrophil infiltration, balances the oxidant-antioxidant status, and regulates the generation of inflammatory mediators to protect tissues.