• Proceedings of the PSK Conference
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• 2000.10a
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• pp.145.2-145.2
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• 2000

• Toxicological Research
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• v.21 no.4
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• pp.303-307
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• 2005

Nanomaterials, which ranges in size from 1 to 100 nm, have been used to create uqnique devices at the nanoscale level possessing novel physical and chemical functional properties. However, the toxicities of nanomaterials have not been fully tested and the risk of nanomaterials is emerging issues in these days. In this study, the cytotoxicity of copper nanoparticles was tested in cultured human bronchial epithelial cells. As a results, copper nanoparticles showed cytotoxicity similar with cupric ion and the apoptotic mechanisms of DNA fragmentation and caspase-3 activation were involved. Induction of heme oxygenase-1 and thioredoxin reductase by copper nanoparticles indicated that cytotoxicity of copper nanoparticles is likely to be mediated through oxidative stress.

• Biomedical Science Letters
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• v.20 no.2
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• pp.56-61
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• 2014

This study attempted to confirm the antioxidative potential of luteolin against tert-butyl hydroperoxide (t-BHP) induced oxidative damage and to investigate its molecular mechanism related to glutathione (GSH)-dependent enzymes in HepG2 cells. Treatment with luteolin resulted in attenuation of t-BHP induced generation of reactive oxygen species (ROS) and oxidative stress-mediated cell death. In addition, accelerated expression of GSH-dependent antioxidative enzymes, glutathione peroxidase (GPx) and glutathione reductase (GR), and heme oxygenase (HO)-1, as well as strengthened GSH content was induced by treatment with luteolin, which was in accordance with increased nuclear translocation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), a transcription factor for phase 2 enzymes, in a dose-dependent manner. These results suggest that the cytoprotective potential of luteolin against oxidative damage can be attributed to fortified GSH-mediated antioxidative pathway and HO-1 expression through regulation of Nrf2 in HepG2 cells.

• CELLMED
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• v.3 no.1
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• pp.1.1-1.7
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• 2013

The present review investigates the role of the cytoprotective enzyme heme oxygenase-1 (HO-1) in human diseases and explores strategies for its clinical use. In recent years, there has been a growing evidence, for the beneficial effects of some phytoconstituents via induction of HO-1 expression, contained in commonly used spices, fruits, and herbs, in preventing various pathologic conditions, including cancer, diabetes, and cardiovascular diseases. HO-1 catalyzes the rate-limiting step in heme catabolism to generate ferrous iron, carbon monoxide, and biliverdin. HO-1 is reported to play crucial roles in cellular protection, such as anti-inflammatory, anti-proliferative and anti-apoptotic effects. These evidences indicate that HO-1 may functions as a potential therapeutic target in various human diseases. The article highlights the current status of the development of the HO-1 modulation pathway using dietary phytoconstituents.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.93-100
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• 2018

Carbon monoxide (CO) is a gaseous molecule produced from heme by heme oxygenase (HO). Endogenous CO production occurring at low concentrations is thought to have several useful biological roles. In mammals, especially humans, a proper neurovascular unit comprising endothelial cells, pericytes, astrocytes, microglia, and neurons is essential for the homeostasis and survival of the central nervous system (CNS). In addition, the regeneration of neurovascular systems from neural stem cells and endothelial precursor cells after CNS diseases is responsible for functional repair. This review focused on the possible role of CO/HO in the neurovascular unit in terms of neurogenesis, angiogenesis, and synaptic plasticity, ultimately leading to behavioral changes in CNS diseases. CO/HO may also enhance cellular networks among endothelial cells, pericytes, astrocytes, and neural stem cells. This review highlights the therapeutic effects of CO/HO on CNS diseases involved in neurogenesis, synaptic plasticity, and angiogenesis. Moreover, the cellular mechanisms and interactions by which CO/HO are exploited for disease prevention and their therapeutic applications in traumatic brain injury, Alzheimer's disease, and stroke are also discussed.

• Journal of Microbiology and Biotechnology
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• v.11 no.1
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• pp.79-84
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• 2001

An aniline-utilizing microorganism identified as a species of Pseudomonas was isolated from soil contaminated highly with aniline and urea-herbicide. This strain was able to utilize aniline as the sole source of carbon and energy, and was shown to harbor a single large plasmid mediating the aniline assimilation. Subsequent plasmid-curing of this bacterium resulted in the abolishment of the aniline utilizing phenotype and the loss of catechol-C2,3O-oxygenase. The reestablishment of the plasmid, denoted pB10, in cured Pseudomonas sp. via filter surface mating, resulted in restoration of the aniline assimilation abilities and enzyme activity.

• Journal of Photoscience
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• v.9 no.3
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• pp.33-36
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• 2002

This study describes RT-PCR and in situ hybridisation protocols, and the immunohistochemical detection method that we have developed to detect and localise cells that express HO-1 in the skin. We found that HO-1 mRNA was absent in normal mouse skin, but after UVA irradiation HO-1 mRNA was expressed in the dermal fibroblasts, and strongly in basal epidermal cells. HO-1 protein was also induced strongly in dermal fibroblasts, and also in epidermal cells. In addition, the HO substrate heme was reduced in skin microsome at 72 hrs post UVA (when HO activity is high). At the same time, the HO products bilirubin and iron levels were elevated in the cutaneous tissue. Thus in addition to a dermal response, there appears to be an epidermal HO response to UVA in vivo that may be relevant for immune modulation by UVA radiation.

• Proceedings of the KACD Conference
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• 2003.11a
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• pp.558-559
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• 2003

Heme oxygenase(HO) is a microsomal enzyme, widely distributed in mammalian tissues, which has a major role in heme metabolism. The role of HO in different tissues has not, as yet, been fully characterized, but it is becoming evident that it is involved in a variety of cellular regulatory and protective mechanism. Therefore, in this report, we confirmed the idea of whether the presence of HO in human pulpal cell, and HO can be a principal mechanism of nitric oxide(NO) mediated pulpal cell damage, by adding a deprivation of NO and to gain clinical relationship. We also accessed the effects of HO in pulpal cells treated with hydrogen.(omitted)

• Proceedings of the Microbiological Society of Korea Conference
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• 1997.04a
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• pp.64.2-64.2
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• 1997

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.149.2-150
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• 2000