Browsing by Author "Bayraktutan, Zafer"

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Determination of Endothelial Nitric Oxide Synthase Gene Polymorphism and Plasma Asymmetric Dimethyl Arginine Concentrations in Patients With Lung Cancer
(Aves, 2020) Bayraktutan, Zafer; Kiziltunc, Ahmet; Bakan, Ebubekir; Alp, Hamit Hakan
Objective: Genetic factors can contribute to both the occurrence and development of lung cancer. This study aimed to investigate endothelial nitric oxide synthase (eNOS) G894T and T-786C polymorphisms and plasma asymmetric dimethylarginine (ADMA) levels of lung cancer patients in comparison with healthy subjects. Materials and Methods: A total of 200 subjects, 100 patients with lung cancer and 100 healthy volunteers were included in this study. To determine eNOS gene polymorphisms, we collected and analyzed blood samples with polymerase chain reaction (PCR). Plasma ADMA levels were evaluated by high-performance liquid chromatography (HPLC). Results: The difference in gene polymorphisms between lung cancer patients and healthy controls were insignificant. However, lung cancer patients had statistically significantly higher plasma ADMA levels than healthy controls. The patients and control groups with CC polymorphisms and TT polymorphisms on eNOS T-786C and G894T gene regions had higher plasma ADMA levels. The CC polymorphisms and plasma ADMA levels were higher in patients with small-cell lung cancer compared to those in patients with non-small-cell lung cancer. Conclusion: Although eNOS gene polymorphisms had no significant difference between lung cancer patients and healthy controls, plasma ADMA levels were higher in lung cancer patients compared to healthy controls. Our study suggests that CC genotypes and elevated plasma ADMA levels might be associated with small-cell lung cancer.
The Relationship Between PDE4 and AQP5 in Lung Tissue Under Inflammatory Conditions: An Experimental Study
(Elsevier, 2026) Bozkurt, Ayse; Bayraktutan, Zafer; Toktay, Erdem; Kara, Adem; Halici, Zekai; Cadirci, Elif
Objective: This study aimed to examine the relationship between Phosphodiesterase 4 (PDE4) and Aquaporin-5 (AQP5) under Lipopolysaccharide (LPS) induced-inflammatory condition. Methods: Inflammatory Acute lung injury (ALI) was induced by intratracheal LPS (5 mg/kg) administration. Rolipram (intraperitoneal) was used as PDE4 inhibiting agent at three different doses (1, 3 and 5 mg/kg) in rat groups. 24 h after LPS administration lung tissues obtained and following analyses performed. AQP5, Phosphodiesterase 4D (PDE4D), Cyclic adenosine monophosphate (cAMP) levels were evaluated for determination of the relationship between these parameters. Also Interleukin-6 (IL-6), Tumor necrosis factor-alpha (TNF-alpha), Nuclear factor kappa B (NF-kappa B), Mitogen-activated protein kinase (MAPK) levels were evaluated as ALI markers. Results: LPS-induced ALI resulted in increased PDE4 enzyme and inflammatory marker levels (IL-6, TNF-alpha, NF-kappa B and MAPK) and decreased AQP5 and cAMP levels. Inhibition of PDE4 enzyme to increase cAMP levels by Rolipram resulted in increased AQP5 expression and decreased inflammatory condition and in lung tissues. These results were supported by histopathological and immunhistochemical results. Conclusion: The fact that this study observed a decreases PDE4 expression and increases in AQP5 expression upon Rolipram administration might indicate a close relationship of these two parameters in inflammatory lung disease.