Master Degree / Yüksek Lisans Tezleri
Permanent URI for this collectionhttps://hdl.handle.net/11147/3008
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Master Thesis Development of Mitochondria Targeted Gold Nanorods(Izmir Institute of Technology, 2019) Uçak, Hande; Özçelik, Serdar; Özçelik, Serdar; 04.01. Department of Chemistry; 04. Faculty of Science; 01. Izmir Institute of TechnologyLung cancer has the largest number of lives for the global pattern of cancer death. However, the percentage of the cancer treatment is too low. Gold nanoparticles have a widely range in terms of biomedical applications in diagnosis, imaging because of their unique optical properties, simple synthesis techniques, biocompatibility and suitable for easy surface change. Redox reactions in the mitochondria generates a potential called as mitochondria membrane potential. The aim of the study is to design mitochondria targeted gold nanorods and to observe how the designed gold nanorods effects the mitochondria membrane potential by targeting the mitochondria on A549 and BEAS-2B cell lines. Gold nanorods were utilized by seed growth mediated method and the surface bioconjugation was performed with triphenyl phosphonium cation as a mitochondria targeted molecule. Poly (sodium-p-styrene sulfonate) was used to prevent aggregation during the bioconjugation process. Gold nanorods which had 30 nm x 10 nm in length and diameter depending on SEM images had well-defined absorption bands 513 nm and 774 nm in wavelength. Mito-pot analysis with the fluorescent intensity ratio and colocalization analysis with light intensity for targeting gold nanorods to mitochondria showed that the accumulation on mitochondria for TPP-GNR was higher than PSSGNR. TPP-GNR was more toxic than PSS-GNR for both of cell lines by investigations of MTT viability test. TPP-GNR targeted to mitochondria and it affected fundamental cellular functions in mitochondria. To concluded that accumulation on mitochondria was accomplished for TPP-GNR and the decreasing of mitochondria membrane potential was observed on this study.Master Thesis Effects of Deleting Mitochondrial Antioxidant Genes on Aging(Izmir Institute of Technology, 2007) Ünlü, Ercan Selçuk; Koç, Ahmet; Koç, Ahmet; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of TechnologyReactive oxygen species (ROS) damage biomolecules, accelerate aging, and shorten life span, whereas antioxidant enzymes mitigate these effects. Because mitochondria are a primary site of ROS generation and also a primary target of ROS attack, they have become a major focus area of aging studies. Here, we employed yeast genetics to identify mitochondrial antioxidant genes that are important for replicative life span. We found that among the known mitochondrial antioxidant genes (TTR1, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, PRX1), deletion SOD1 (Cu, Zn superoxide dismutase), SOD2 (Manganese-containing superoxide dismutase), and CCS1 (Copper chaperone), shortened the life span enormously under normal conditions. The life span decreased 40% for sod1 mutant, 72% for sod2 mutant, and 50% for ccs1 mutant. When a respiratory carbon source was used in addition to sod1, sod2 and ccs1, deletion of CCP1 (cytocrome c peroxidase) also lead to a decrease in life span which decreased% 79 for sod1 mutant, 87 % for sod2 mutant, 51 % for ccs1 and65 % for ccp1 mutant. Deletion of the other genes had little or no effect on life span for both conditions. To further investigate the role of these antioxidant genes molecular damages on lipids, proteins, and DNA were detected in mutants. The results showed that level of lipid peroxidation was usually lower when cells were grown under normal conditions. If cells were grown in respiratory substrate glycerol, deletion of CCS1, SOD2, GRX2, CCP1, TRR2 and PRX1 genes increased cellular lipid peroxidation levels by 87%, 73%, 65, 48%, 30% and 16% respectively. Protein carbonylation levels were 34% higher for ccp1 and 87% higher for grx2 mutants compared to WT cells when the cells were grown under normal conditions. However, it increased 65% for ccs1, 61% for prx1, 57% for glo4, 55% for ccp1, 49% for sod1, 37% for sod2, 33% for grx2, 18% for trx3, 17% for grx5 and 7% for trr2 when the cells were grown in the presence of glycerol. Q-PCR assay showed that deletion of CCS1 and PRX1 lead to DNA damages in mitochondrial DNA. Our overall results showed that some of the antioxidant mitochondrial mutants lived shorter and accumulated extensive molecular damages in the presence of respiratory carbon source.Master Thesis Identification of Mitochondrial Electron Transport Chain Mutations That Effect Ageing(Izmir Institute of Technology, 2009) Hacıoğlu, Elise; Koç, Ahmet; Koç, Ahmet; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of TechnologyAging can be defined as the loss of cell functionality by accumulation of deleterious effects. Mitochondrial electron transport chain (ETC) is the main site for reactive oxygen species (ROS) production. According to free radical theory of aging, free radicals produced by normal aerobic respiration accumulate by time and can cause aging. Although previous studies have identified that inner mitochondrial membrane complexes I and III are the major sites of ROS production, role of ETC genes in ROS production is a matter of debate. The purpose of the present study was to determine the ETC mutations that affect aging using S.cerevisiae as a model organism. Deletion mutants of S.cerevisiae lacking 73 genes of ETC were analyzed aging and we found out that nine mutants caused reduction in replicative lifespan. In addition to aging profiles, ROS production levels, respiratory competence and oxidative stress tolerance level of these deletion strains were also investigated. In order to verify lifespan modulation by these genes, they were all overexpressed in wild-type cells and aging profile of these cells was analyzed. Most of the cells lived longer than wild type control cells containing sham vector. Our results suggest that some of the ETC genes play important roles in mitochondrial functions and aging. We hope that our results will contribute to the field of aging studies.