Browsing by Author "Bolukbas, Cengiz"

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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.