Yazar "Oztas, E" seçeneğine göre listele

Listeleniyor 1 - 3 / 3
  • Küçük Resim Yok
    Öğe
    Effects of electromagnetic radiation from a cellular telephone on epidermal Merkel cells
    (Blackwell Munksgaard, 2003) Irmak, MK; Oztas, E; Yagmurca, M; Fadillioglu, E; Bakir, B
    The number of reports on the effects induced by electromagnetic radiation (EMR) from cellular telephones in various cellular systems is still increasing. Until now, no satisfactory mechanism has been proposed to explain the biological effects of this radiation except a role suggested for mast cells. Merkel cells may also play a role in the mechanisms of biological effects of EMR. This study was undertaken to investigate the influence of EMR from a cellular telephone (900 MHz) on Merkel cells in rats. A group of rats was exposed to a cellular telephone in speech position for 30 min. Another group of rats was sham-exposed under the same environmental conditions for 30 min. Exposure led to significantly higher exocytotic activity in Merkel cells compared with the sham exposure group. This finding may indicate the possible role of Merkel cells in the pathophysiology of the effects of EMR.
  • Küçük Resim Yok
    Öğe
    Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats
    (Elsevier Science Inc, 2004) Ilhan, A; Akyol, O; Gurel, A; Armutcu, F; Iraz, M; Oztas, E
    Because oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase. (C) 2004 Elsevier Inc. All rights reserved.
  • Küçük Resim Yok
    Öğe
    Protective effects of caffeic acid phenethyl ester on doxorubicin-induced cardiotoxicity in rats
    (Wiley, 2004) Fadillioglu, E; Oztas, E; Erdogan, H; Yagmurca, M; Sogut, S; Ucar, M; Irmak, MK
    The prevention of doxorubicin (DXR)-induced cardiotoxicity may be helpful to improve future DXR therapy. The aim of this study was to investigate the cardio-protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on DXR-induced cardiotoxicity. Rats were divided into three groups and treated with saline, DXR and DXR + CAPE. Rats were treated with CAPE (10 gmol kg(-1) day(-1) i.p.) or saline starting 2 days before a single dose of DXR (20 mg kg(-1) i.p.). Ten days later, haemodynamic measurements were performed and the hearts were excised for biochemical analyses and microscopic examination. The heart rate and mean blood pressure were higher and the pulse pressure was lower in the DXR group than in the other two groups. The administration of DXR alone resulted in higher myeloperoxidase activity, lipid peroxidation and protein carbonyl content than in the other groups. The activities of superoxide dismutase and catalase were higher in DXR and DXR + CAPE groups than in the saline group. Rats in the DXR + CAPE group had increased catalase activity in comparison with the DXR group and high glutathione peroxidase activity in comparison with the other two groups. There was severe disruption of mitochondrial fine structure in the electron microscopy of the DXR group. In contrast, myocardial microscopy appeared nearly normal in the DXR + CAPE group (as defined at the electron microscopic level). In light of these in vivo haemodynamic, enzymatic and morphological results, we conclude that CAPE pretreatment significantly attenuated DXR-induced cardiac injury, possibly with its antioxidant effects. Copyright (C) 2004 John Wiley Sons, Ltd.