Person:
OKTAY, NİHAL ŞEHKAR

Profile Picture

Email Address

Birth Date

Research Projects

Organizational Units

OrgUnit Logo
Organizational Unit

Job Title

Last Name

OKTAY

First Name

NİHAL ŞEHKAR

Name

Filters

2016 - 20182
Reset filters

Settings

Author: ALTURFAN, EBRU IŞIK × Subject: ACID ×

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    PublicationOpen Access
    Edaravone Ameliorates Valproate-Induced Gingival Toxicity by Reducing Oxidative-Stress, Inflammation and Tissue Damage
    (MARMARA UNIV, FAC MEDICINE, 2016-05-10) YARAT, AYŞEN; Oktay, Sehkar; Alev, Burcin; Koc Ozturk, Leyla; Tunali, Sevim; Demirel, Sezin; Emekli Alturfan, Ebru; Tunali-Akbay, Tugba; Akyuz, Serap; Yanardag, Refiye; Yarat, Aysen
    Valproic acid (2-n-propylpentanoic acid, VPA), the most widely used antiepileptic drug, has potential adverse effects and it can disrupt the oxidant and antioxidant balance. Edaravone (3-methyl-1-phenyl-2-pyrazoline-5-one, EDA) is a potent free radical scavenger. In this study, the effect of EDA on gingiva in VPA induced toxicity was investigated. Female Sprague Dawley rats were randomly divided into four groups: control group, EDA (30 mg/kg/day) given group, VPA (0.5 g/kg/day) given group, and VPA+EDA (in same dose and time) given group. EDA and VPA were given intraperitoneally for seven days. Total protein, lipid peroxidation (LPO), sialic acid (SA) and reduced glutathione (GSH) levels and catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), myeloperoxidase (MPO), alkaline phosphatase (ALP), acid phosphatase (ACP), sodium potassium ATPase (Na+/K+-ATPase) and tissue factor (TF) activities were determined in gingiva homogenates. The VPA-induced increases were statistically significant for MPO (p<0.01), ACP (p<0.01), Na+/K+-ATPase (p<0.05) and TF (p<0.01) activities, but not for LPO level and ALP activities. EDA treatment markedly blunted all such elevated anomalies. Conclusively, VPA induced oxidative and inflammatory gingival tissue damage, reactions that were appreciably reversed by concurrent administration of EDA.
  • No Thumbnail Available
    PublicationMetadata only
    The effect of vitamin U on the lung tissue of pentyleneterazole-induced seizures in rats
    (SPRINGER, 2018) YARAT, AYŞEN; Oktay, Sehkar; Bayrak, Gamze; Alev, Burcin; Ipekci, Hazal; Ustundag, Unsal Veli; Turkyilmaz, Ismet Burcu; Pisiriciler, Rabia; Emekli-Alturfan, Ebru; Tunali-Akbay, Tugba; Yanardag, Refiye; Yarat, Aysen
    The aim of this study is to investigate the therapeutic effects of vitamin U (Vit U) on lung tissue of pentyleneterazole (PTZ)-induced seizures in rats. Sprague Dawley male rats were randomly divided into four groups as follows: control (0.9% NaCl given, intraperitoneally); Vit U (50 mg/kg/day, for 7 days by gavage); PTZ; (60 mg/kg one dose, intraperitoneally); and PTZ + Vit U (in same dose and time). At the end of the experiment, lung tissues were taken and examined biochemically and cytologically. Lipid peroxidation (LPO), glutathione (GSH), sialic acid (SA), and nitric oxide (NO) levels, and superoxide dismutase (SOD) and catalase (CAT) activities were determined in lung homogenates. Imprinted lung samples were stained with May Grunwald-Giemsa stain and microscopically examined for the presence of collagen fibers, macrophage, leucocyte, and epithelial cells. PTZ administration significantly increased GSH level and CAT activity and significantly decreased SOD activity compared to the control group. Vit U administration significantly increased GSH level and CAT activity compared to the control group. GSH and NO levels significantly decreased in PTZ + Vit U group compared to the PTZ group. In cytologic analysis, increased collagen fibers, macrophages, leucocytes, and epithelial cells were observed in PTZ group compared to the control group, and Vit U administration decreased these cytological parameters compared to the PTZ group. The findings of this study support the possible protective role of using Vit U as an add-on therapy in order to prevent lung tissue injury which may occur during seizures in epilepsy.