Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7148
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Article Citation - WoS: 1Citation - Scopus: 1Bioavailability Assessment of the Novel Gsh-Functionalized Feb Nanoparticles Via Oxidative Stress and Trace Element Metabolism in Vitro: Promising Tools for Biomedical Applications(Springer, 2024) Aydemir, Duygu; Aribuga, Dilara; Hashemkhani, Mahshid; Acar, Havva Yagci; Çağıran, Özge Balcı; Ulusu, Nuriye NurayIron-based magnetic nanoparticles (NPs) have attracted significant attention in biomedical research, particularly for applications such as cancer detection and therapy, targeted drug delivery, magnetic resonance imaging (MRI), and hyperthermia. This study focuses on the synthesis and glutathione (GSH) functionalization of iron boride (FeB) nanoparticles (NPs) for prospective biomedical use. The GSH-functionalized FeB NPs (FeB@GSH) demonstrated ferromagnetic behavior, with a saturation magnetization (Ms) of 45.8 emu/g and low coercivity (Hc = 1000 Oe), indicating desirable magnetic properties for biomedical applications. Transmission electron microscopy (TEM) analysis of the FeB@GSH revealed well-dispersed nanoparticles with diameters smaller than 30 nm. Comprehensive nanotoxicity and biocompatibility assessments were performed using various healthy and cancer cell lines, including 293 T, HeLa, 3T3, MCF7, HCT116, and CFPAC-1. Cytotoxicity assays were conducted on FeB@GSH-treated cells over a dose range of 0-300 mu g/mL during 24-h incubations. Results indicated no significant differences in cell viability between treated and untreated control groups, confirming the biocompatibility of FeB@GSH. Further nanotoxicity evaluations were carried out on 3T3, 293 T, and CFPAC-1 cell lines, focusing on oxidative stress markers and cellular metabolism by measuring antioxidant enzyme activity. Additionally, ion release and mineral metabolism were assessed using inductively coupled plasma mass spectrometry (ICP-MS), revealing no notable variations between the treated and control groups. These findings suggest that FeB@GSH NPs exhibit excellent biocompatibility, making them promising candidates for diverse biomedical applications, including medical imaging, drug delivery systems, and therapeutic interventions.Article Citation - WoS: 19Citation - Scopus: 22Absence of Superoxide Dismutase Activity Causes Nuclear Dna Fragmentation During the Aging Process(Academic Press Inc., 2014) Muid, Khandaker Ashfaqul; Karakaya, Hüseyin Çaglar; Koç, AhmetSuperoxide dismutases (SOD) serve as an important antioxidant defense mechanism in aerobic organisms, and deletion of these genes shortens the replicative life span in the budding yeast Saccharomyces cerevisiae. Even though involvement of superoxide dismutase enzymes in ROS scavenging and the aging process has been studied extensively in different organisms, analyses of DNA damages has not been performed for replicatively old superoxide dismutase deficient cells. In this study, we investigated the roles of SOD1, SOD2 and CCS1 genes in preserving genomic integrity in replicatively old yeast cells using the single cell comet assay. We observed that extend of DNA damage was not significantly different among the young cells of wild type, sod1Δ and sod2Δ strains. However, ccs1Δ mutants showed a 60% higher amount of DNA damage in the young stage compared to that of the wild type cells. The aging process increased the DNA damage rates 3-fold in the wild type and more than 5-fold in sod1Δ, sod2Δ, and ccs1Δ mutant cells. Furthermore, ROS levels of these strains showed a similar pattern to their DNA damage contents. Thus, our results confirm that cells accumulate DNA damages during the aging process and reveal that superoxide dismutase enzymes play a substantial role in preserving the genomic integrity in this process.Article Citation - WoS: 18Citation - Scopus: 19Assessment of Chronological Lifespan Dependent Molecular Damages in Yeast Lacking Mitochondrial Antioxidant Genes(Elsevier Ltd., 2010) Demir, Ayşe Banu; Koç, AhmetThe free radical theory of aging states that oxidative damage to biomolecules causes aging and that antioxidants neutralize free radicals and thus decelerate aging. Mitochondria produce most of the reactive oxygen species, but at the same time have many antioxidant enzymes providing protection from these oxidants. Expecting that cells without mitochondrial antioxidant genes would accumulate higher levels of oxidative damage and, therefore, will have a shorter lifespan, we analyzed oxidative damages to biomolecules in young and chronologically aged mutants lacking the mitochondrial antioxidant genes: G. RX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, and PRX1. Among these mutants, ccp1Δ, trx3Δ, grx5Δ, prx1Δ, mutants were sensitive to diamide, and ccs1Δ and sod2Δ were sensitive to both diamide and menadione. Most of the mutants were less viable in stationary phase. Chronologically aged cells produced higher amount of superoxide radical and accumulated higher levels of oxidative damages. Even though our results support the findings that old cells harbor higher amount of molecular damages, no significant difference was observed between wild type and mutant cells in terms of their damage content. © 2010 Elsevier Inc.