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Article Citation - WoS: 7Citation - Scopus: 6A platinum blue complex exerts its cytotoxic activity via DNA damage and induces apoptosis in cancer cells(Wiley, 2017) Adiguzel, Zelal; Ozalp-Yaman, Seniz; Celik, Gokalp; Salem, Safia; Bagci-Onder, Tugba; Senbabaoglu, Filiz; Acilan, CeydaHere, we describe the characteristics of a Pt-blue complex [Pt-4(2-atp)(8)(H2O)(OH)] (2-atp: 2-aminothiophenol) as a prodrug for its DNA-binding properties and its use in cancer therapy. The nature of the interaction between the Pt-blue complex and DNA was evaluated based on spectroscopic measurements, the electronic absorption spectra, thermal behavior, viscosity, fluorometric titration, and agarose gel electrophoresis. Our results suggested that the compound was able to partially intercalate DNA and appeared to induce both single- and double-stranded breaks (DBS) on DNA in vitro, but no DSBs in cells. The ability of the compound to induce DNA damage was dependent on reactive oxygen species (ROS) in vitro. There was also elevated formation of ROS and SOD expression in response to drug treatment in cell culture. The complex was found to be more cytotoxic to cancer cells in comparison with noncancer controls using WST-1 assay. The mean of cell death was determined to be apoptosis as assessed via biochemical, morphological, and molecular observations, including DNA condensation/fragmentation analysis, live cell imaging microscopy, TUNEL analyses, and increase in the levels of pro-apoptotic genes such as Bag3, Bak, Bik, Bmf, and Hrk. Hence, the Pt-blue complex under study grants premise for further studies.Article Citation - WoS: 1Citation - Scopus: 1Dietary Total Antioxidant Capacity and Oxidative Stress in Patients With Type-2 Diabetes(Mattioli 1885, 2021) Cetiner, Ozlem; Sendur, Suleyman Nahit; Yalcin, Tuba; Bayraktar, Miyase; Rakicioglu, NeslisahBackground: Reactive oxygen species can disrupt normal cellular functions by damaging DNA, protein, and lipid structures of the cell. Some antioxidant molecules may protect the body against reactive oxygen species. We aimed to investigate the relationship between the dietary intake of antioxidants and oxidative DNA damage in diabetic patients. Material and Methods: A total of 85 individuals were included in the study, of which 30 were newly diagnosed with type-2 diabetes, 30 were formerly diagnosed with type-2 diabetes, and 25 were healthy individuals. Twenty-four-hour dietary recalls were recorded for 3 consecutive days. Dietary total antioxidant capacity and dietary oxidative balance scores were calculated according to these records. Spot urine samples were collected and analyzed for 8-hydroxy-2' deoxyguanosine/creatinine. Results: Dietary total antioxidant capacity, estimated via different methods, was higher in the controls than that in patients with type-2 diabetes (p<0.05). The urinary 8-hydroxy-2'-deoxyguanosine/creatinine ratio, a reliable predictor of oxidative DNA damage, was also higher in non-diabetic patients (p<0.05). The urinary 8-hydroxy-2'-deoxyguanosine/creatinine ratio was not related to dietary antioxidant intake (p>0.05). Conclusion: Urinary 8-hydroxy-2'-deoxyguanosine/creatinine concentration may not always reflect the current oxidative status of the body.
