PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7645
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Article Citation - WoS: 3Citation - Scopus: 4Comparison of the Effects of Statins on A549 Nonsmall-Cell Lung Cancer Cell Line Lipids Using Fourier Transform Infrared Spectroscopy: Rosuvastatin Stands Out(Wiley, 2021) Aksoy, Hatice Nurdan; Ceylan, ÇağatayStatins are commonly prescribed antilipidemic and anticholesterol class of drugs. In addition to their major role, they have been found to have anticancer effects on in vitro, animal and clinical studies. The aim of this study was to investigate the effects of six different statins (rosuvastatin, pravastatin, simvastatin, lovastatin, fluvastatin, and atorvastatin) on A549 cancer cells lipids by Fourier transform infrared (FTIR) spectroscopy. Proliferation tests were carried out to detect the half-maximal inhibitory concentrations (IC50) of each statin on A549 cells. The IC50 values were 50 mu M for simvastatin, 150 mu M for atorvastatin and pravastatin, and 170 mu M for fluvastatin, 200 mu M for rosuvastatin and lovastatin on A549 cells. No correlation was found between the antiproliferative effects of the statins and lipid-lowering effect. The cells were treated with IC5, IC10, and IC50 values of each statins concentration and lipid extracts were compared using FTIR spectroscopy. The results indicated that different statins had different effects on the lipid content of A549 cells. The FTIR spectra of the lipid exctracts of statin-treated A549 cells indicated that the value of hydrocarbon chain length, unsaturation index, oxidative stress level, and phospholipid containing lipids increased except for rosuvastatin-treated A549 cells. In addition, rosuvastatin significantly lowered cholesterol ester levels. In conclusion, the contrasting effects of rosuvastatin should be further investigated.Article Citation - WoS: 6Citation - Scopus: 6A Molecular and Biophysical Comparison of Macromolecular Changes in Imatinib-Sensitive and Imatinib-Resistant K562 Cells Exposed To Ponatinib(SAGE Publications Inc., 2016) Kartal Yandım, Melis; Ceylan, Çağatay; Elmas, Efe; Baran, YusufChronic myeloid leukemia (CML) is a type of hematological malignancy that is characterized by the generation of Philadelphia chromosome encoding BCR/ABL oncoprotein. Tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, and dasatinib, are used for the frontline therapy of CML. Development of resistance against these TKIs in the patients bearing T315I mutation is a major obstacle in CML therapy. Ponatinib, the third-generation TKI, is novel drug that is effective even in CML patients with T315I mutation. The exact mechanism of ponatinib in CML has been still unknown. In this study, we aimed to determine the potential mechanisms and structural metabolic changes activated by ponatinib treatment in imatinib-sensitive K562 human CML cell lines and 3 μM-imatinib-resistant K562/IMA3 CML cell lines generated at our lab. Apoptotic and antiproliferative effects of ponatinib on imatinib-sensitive and 3 μM-imatinib-resistant K562/IMA3 CML cells were determined by proliferation and apoptosis assays. Additionally, the effects of ponatinib on macromolecules and lipid profiles were also analyzed using Fourier transform infrared spectroscopy (FTIR). Our results revealed that ponatinib inhibited cell proliferation and induced apoptosis as determined by loss of mitochondrial membrane potential, increased caspase-3 enzyme activity, and transfer of phosphatidylserine to the plasma membrane in both K562 and K562/IMA-3 cells. Furthermore, cell cycle analyses revealed that ponatinib arrested K562 and K562/IMA-3 cells at G1 phase. Moreover, ponatinib treatment created a more ordered nucleic acid structure in the resistant cells. Although the lipid to protein ratio increased in imatinib-sensitive K562 cells with a little decrease in the K562/IMA-3 cells, ponatinib treatment indicated significant changes in the lipid composition such as a significant increase in the cellular cholesterol amounts much more in the K562/IMA-3 cells than the sensitive counterparts. Unsaturation in lipids was higher in the resistant cells; however, increases in lipids without phosphate and the number of acyl chains were much higher in the K562 cells. Taken together, all these results showed powerful antiproliferative and apoptotic effects of ponatinib in both imatinib-sensitive and imatinib-resistant CML cells in a dose-dependent manner, and hence, the use of ponatinib for the treatment of TKI-resistant CML patients may be an effective treatment approach in the clinic. More importantly, these results showed that FTIR spectroscopy can detect drug-induced physiological changes in cancer drug resistance.Article Citation - WoS: 11Citation - Scopus: 9Biophysical Evaluation of Physiological Effects of Gilthead Sea Bream (sparus Aurata) Farming Using Ftir Spectroscopy(Elsevier Ltd., 2014) Ceylan, Çağatay; Tanrıkul, Tansel; Özgener, HüseyinSparus aurata is one of the two most important cultured fish species in the Mediterranean region. The present work investigates the effects of culturing in S. aurata liver tissue at the molecular level using Fourier Transform Infrared (FTIR) spectroscopy. FTIR spectroscopy revealed dramatic differences between the wild and aquacultured fish liver cells, which mainly indicated that the level of glycogen increased in the aquacultured samples and the protein/lipid ratio decreased by 42.29% indicating that triglycerides and cholesterol esters increased and the protein content decreased in the aquacultured samples. The 15.99% increase in the level of unsaturation indicated elevated lipid peroxidation. Structural/organisational changes in the nucleic acids along with increased transcriptional status of the liver tissue cells were observed in the cultured fish tissue. All these results indicated that culturing induces significant changes in fish physiology. In addition FTIR spectroscopy is a promising method to monitor the physiological changes in fish physiology.