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Ivy geranium (Pelargonium peltatum) is a heat susceptible species with its heat tolerance varying among varieties. Reactive oxygen species (ROS) and in-vivo defense systems are related to plant heat damage and heat tolerance. Application of chelated-iron has also been reported to enhance ivy geranium heat tolerance; however, the correlation of ROS, relative enzyme stability, and iron content to differences in heat tolerance in ivy geraniums is unknown. Here we show that the H2O2 content and ROS scavenging enzyme stability in ivy geranium varies with varieties and active iron is not related to heat tolerance in ivy geranium. H2O2 content in mature leaves in both heat tolerant 'Beach' and sensitive 'Butterfly' increased under heat stress, but 'Butterfly' had a relatively greater increase of this toxic compound. Catalase (CAT) activities in young leaves in both varieties decreased. In young leaves of 'Butterfly', CAT activities decreased to a level significantly lower than that in old leaves while this did not occur in 'Beach'. Superoxide dismutase (SOD) activities in 'Butterfly' young leaves were also decreased. All these phenomenon coincided with the heat tolerance differences of the two varieties. Active iron content only changed with leaf age and did not vary between varieties or treatments. Our results demonstrated that ROS scavenging ability and relative enzyme stability may indicate heat tolerance in ivy geranium and that iron deficiency was not the cause of heat damage. Cell Membrane Themostability (CMT) and Triphenyl Tetrazolium Chloride (TTC) cell viability tests are alternative, laboratory-based screening methods for screening for heat-tolerance. Both CMT and TTC tests can represent the variance in heat tolerance observed in ivy geraniums. The results of both CMT and TTC tests correlated well with plant width and growth indexes although their correlations to plant chlorosis were low. Unlike TTC, CMT strongly correlated with plant width. CMT and TTC tests are complementary laboratory-based methods that can be applied to cultivar screening for heat tolerance in ivy geraniums.

京都大学 / 新制・課程博士 / 博士(医科学) / 甲第24141号 / 医科博第142号 / 新制||医科||9(附属図書館) / 京都大学大学院医学研究科医科学専攻 / (主査)教授 松田 道行, 教授 斎藤 通紀, 教授 妹尾 浩 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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Cancer cells adapt to high levels of oxidative stress in order to survive and proliferate, making the transcription factors involved in antioxidant defence regulation targets of interest. The transcription factor NF E2 Related Factor 2 (NRF-2) regulates cellular defence genes including those encoding intracellular redox-balancing proteins such as enzymes involved in glutathione metabolism. Glutathione in particular is an important intracellular antioxidant molecule. NRF-2 binds to the Antioxidant Response Element (ARE) in the promoter of its target genes. Under basal conditions, Kelch-like ECH-associated protein 1 (KEAP1) acts as an inhibitor that targets NRF-2 for ubiquitination. During oxidative stress, NRF-2 dissociates from KEAP1 and enters the nucleus to bind to the ARE sequence. It is hypothesized that the elevated Reactive Oxygen Species may be depleting the glutathione levels within the cancer cell. System xc- is a cystine/glutamate antiporter that exports glutamate while importing cystine to synthesize glutathione. In response to oxidative stress, the cells increase system xc- activity in order to provide cystine for glutathione synthesis. There is evidence that expression of xCT, the specific subunit of system xc-,is regulated by NRF-2. However this has not yet been demonstrated in human breast cancer cells, which is the focus of this project. Basal expression of NRF-2, KEAP1 and xCT was characterized in three breast cancer cell lines (MDA-MB-231, MCF-7 and T47D) and compared to two non-cancer cell lines (184B5 and MCF10A). Basal protein levels of NRF-2 and KEAP1 showed no differences between cell lines. Basal protein levels of xCT were increased in MCF10A cells than T47D cells. MCF-7 cells were treated with hydrogen peroxide (H2O2) resulting in NRF-2 protein accumulation in the nucleus. With H2O2 treatment, xCT mRNA levels increased in MCF-7 cells. Additionally, transient overexpression of NRF-2 increased extracellular glutamate levels in MCF-7 cells. These data support a model that under oxidative stress, NRF-2 is localized to the nucleus and transcriptionally upregulates xCT. This is the first study in which the regulation of xCT has been linked to oxidative stress via NRF-2 in human breast cancer cells. / Thesis / Master of Science (MSc)

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Macrophages are a cornerstone in innate immunity, especially important in detecting and killing invading microorganisms. In tumor biology, the macrophages can contribute both to anti-tumor activity and tumor promotion depending on individual tumor microenvironment and therefore have a large impact on both tumor progression and prognosis. Two of the most important functions of macrophages are the ability to phagocytose microorganisms and then kill them through the respiratory burst. Phagocytosis activates the respiratory burst, but the more subtle interactions between these processes are less known. Since phagocytosis and reactive oxygen species production are two attributes that change between the classically and alternatively activated macrophages we decided to compare these two functions in macrophages. Activation of macrophages varies in terms of stimuli and effects. We specifically looked at macrophage activation by tumor cell lines and by chemical stimulation due to caffeine. We hypothesized that the level of oxidation would be directly linked to the level of phagocytosis. We assume that caffeine will increase activity in macrophages and that tumor cell co-incubation will decrease it. We found that there is a high correlation between the level of engulfment and level of respiratory burst. Chemical stimulation with caffeine can lower aggressiveness of macrophages at lower concentration, raise it at higher concentrations and eventually become toxic to the cell. Co-incubation with leukemic cell lines, as well with necrotic cells, affected an increase in aggressiveness.