Browsing by Author "Kocyigit, Abdurrahim"

Now showing 1 - 4 of 4

Effects of Cichorium Intybus Extract on Seizure Development, Bcl-2, Siklin B1 Ve Β-Tubulin Levels in Pentylenetetrazole-Kindling Model of Epilepsy in Rats
(Wiley-blackwell, 2015) Erkec, Ozlem Ergul; Meral, Ismail; Kara, Mehmet; Kocyigit, Abdurrahim; Armagan, Metin; Ozer, Omer Faruk
Peripheral Lymphocyte Dna Damage and Oxidative Status After Eradication Therapy in Patients Infected With Helicobacter Pylori
(Medycyna Praktyczna, 2011) Dulger, Ahmet C.; Aslan, Mehmet; Nazligul, Yasar; Horoz, Mehmet; Bolukbas, Cengiz; Bolukbas, Fusun F.; Kocyigit, Abdurrahim
Introduction Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. Objectives The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. Patients and methods The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. Results The total antioxidant status (TAS) was lower in Hp+ patients than in Hp-patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). Conclusions Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.
Peripheral Lymphocyte Dna Damage and Oxidative Stress in Patients With Ulcerative Colitis
(Medycyna Praktyczna, 2011) Aslan, Mehmet; Nazligul, Yasar; Bolukbas, Cengiz; Bolukbas, Fusun F.; Horoz, Mehmet; Dulger, Ahmet C.; Kocyigit, Abdurrahim
Introduction Ulcerative colitis (UC) is a fairly common chronic inflammatory disorder. Chronic inflammation may contribute to the risk of colorectal cancer through the accumulation of specific products resulting from DNA damage. Previous studies reported that DNA damage and oxidative stress play a significant role in the pathophysiology of UC, but the results are inconsistent. Objectives In the present study, we investigated peripheral DNA damage and oxidative stress in patients with UC. Patients and methods The study included 20 patients with UC and 20 controls. Peripheral lymphocyte DNA damage was measured using the alkaline comet assay. Plasma total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. Results DNA damage levels, TOS, and OSI were significantly higher in patients with UC than in controls (P < 0.001 for all para-meters), while TAC was significantly lower (P < 0.001). DNA damage was significantly correlated with TOS, TAC, and OSI (r = 0.604, P < 0.001; r = -0.593, P < 0.001; and r = 0.716, P < 0.001, respectively). Moreover, TAC levels were significantly correlated with TOS and OSI (r = 0.604, P < 0.001; r = -0.399, P < 0.05; and r = -0.513, P < 0.05, respectively). Conclusions Our results show that increased peripheral DNA damage and oxidative stress seem to be associated with decreased antioxidant levels and thus may in part contribute to the development of colorectal cancer associated with UC.
Peripheral Mononuclear Leukocyte Dna Damage, Plasma Prolidase Activity, and Oxidative Status in Patients With Benign Prostatic Hyperplasia
(Taylor & Francis Ltd, 2015) Gecit, Ilhan; Meral, Ismail; Aslan, Mehmet; Kocyigit, Abdurrahim; Celik, Hakim; Taskin, Abdullah; Ceylan, Kadir
Objectives: Prolidase plays a major role in collagen turnover, matrix remodeling, and cell growth. Benign prostatic hyperplasia (BPH) may be associated with an increased extracellular matrix deposition. Therefore, the present study was designed to investigate the plasma prolidase activity, oxidative status, and peripheral mononuclear leukocyte DNA damage in patients with BPH. Patients and methods: Twenty-six male patients with BPH and 24 healthy male subjects were included in this study. Blood samples were collected from antecubital vein after an overnight fasting period, and the plasma was separated. Plasma prolidase activity, total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. The peripheral lymphocyte oxidative DNA damage was determined using an alkaline single cell gel electrophoresis assay (comet assay). Results: The plasma prolidase activity, TOS levels, OSI values, and peripheral mononuclear leukocyte DNA damage were significantly higher (P < 0.001), while the TAC levels were significantly lower (P < 0.001) in patients with BPH than controls. In BPH patients, the prolidase activity was significantly associated with TAC levels (r = -0.366, P < 0.05), TOS levels (r = 0.573, P < 0.001), and OSI (r = 0.618, P < 0.001) and peripheral mononuclear leukocyte DNA damage (r = 0.461, P < 0.001). Conclusions: Our results showed that BPH might be associated with an increased oxidative stress, and also an increased plasma prolidase activity. Increased prolidase activity might play an important role in the etiopathogenesis and/or progression of BPH.