• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2001.05a
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• pp.128-128
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• 2001

Atrazine, one of herbicide widely used in agriculture, is classified as a possible human carcinogen (2B group) that may cause breast and ovarian cancers by IARC, and is known as an endocrine disrupter. Atrazine has been subjected to broad ranges of genotoxicity tests wi th predominantly negative results, but reported conflicting results across two or more independent tests as well. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.200-200
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• 2002

Cadmium (Cd) is an environmental pollutant and categorized as a human carcinogen, which has a tendency to accumulate in the human body. The level of Cd in renal cortex and liver are good indicators as an index of Cd exposure in general population. Geometric mean concentration of Cd is 27.4 and 3.1 /g wet weight in renal cortex and liver, respectively, in Korean. Cd is toxic to a number of tissues, notably the liver, kidney, testis, lung, lymphoid tissue and lung. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.183-183
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• 2001

Atrazine, one of herbicide widely used in agriculture, is classified as a possible human carcinogen (2B group) that may cause breast and ovarian cancers by IARC, and is known as an endocrine disruptor. Atrazine has been subjected to broad ranges of genotoxicity tests with predominantly negative results, but reported conflicting results across two or more independent tests as well. This fact indicates that a more comprehensive genotoxicity assessment needs for atrazine.(omitted)

• The Korean Journal of Pharmacology
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• v.21 no.1
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• pp.12-26
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• 1985

The generation of $O^{-}_{2}{\cdot}$ and its toxic effects were studied with rat brain mitochondria. The production of $O^{-}_{2}{\cdot}$ from mitochondria in the presence of succinate and antimycin was demonstrated by SOD-inhibitable reduction of NBT. Although succinate can support the $O^{-}_{2}{\cdot}$ formation, the highest rate needs antimycin indicating that blockade of electron flow in the respiratory chain augments the univalent reduction of molecular oxygen. Under this condition, $H_2O_2$ was also observed to be produced. But its formation appears to be derived from the dismutation of the primary product, $O^{-}_{2}{\cdot}$ since the rate of $H_2O_2$ production was markedly decreased by NBT and ferricytochrome c. The $O^{-}_{2}{\cdot}$ and $H_2O_2$ produced were able to cause toxic actions to mitochondrial and extra-mitochondrial components as shown by lipid peroxidation of mitochondrial membrane, and inactivation and lysis of isocitrate dehydrogenase and erythrocytes added to the medium, respectively. In all the toxic actions observed, $Fe^{++}$ was required. It appears that in the toxic actions $OH{\cdot}$ generated from the iron-catalyzed Haber-Weiss reaction acts as a mediator. This was supported by the finding that mitochondria in the presence of succinate and antimycin produced ethylene from methional, and $Fe^{++}$ added increased the ethylene production. The observed toxic actions of mitochondrial $O^{-}_{2}{\cdot}$ may provide evidence supporting a potential role of mitochondria as a source of oxygen radicals to cause tissue damage.

• Toxicological Research
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• v.29 no.3
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• pp.149-155
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• 2013

G protein-coupled receptors (GPCRs) are membrane receptors; approximately 40% of drugs on the market target GPCRs. A precise understanding of the activation mechanism of GPCRs would facilitate the development of more effective and less toxic drugs. Heterotrimeric G proteins are important molecular switches in GPCR-mediated signal transduction. An agonist-activated receptor interacts with specific sites on G proteins and promotes the release of GDP from the $G{\alpha}$ subunit. Because of the important biological role of the GPCR-G protein coupling, conformational changes in the G protein upon receptor coupling have been of great interest. One of the most important questions was the interface between the GPCR and G proteins and the structural mechanism of GPCR-induced G protein activation. A number of biochemical and biophysical studies have been performed since the late 80s to address these questions; there was a significant breakthrough in 2011 when the crystal structure of a GPCR-G protein complex was solved. This review discusses the structural aspects of GPCR-G protein coupling by comparing the results of previous biochemical and biophysical studies to the GPCR-G protein crystal structure.

• Toxicological Research
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• v.25 no.1
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• pp.35-40
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• 2009

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and related halogenated aromatic hydrocarbons elicit a diverse spectrum of biochemical and toxic responses in laboratory animals and mammalian cells in culture. Toxicity and carcinogenicity of TCDD is well established but the molecular mechanism is still poorly understood. Here, we found the noble responsive genes to TCDD using the differential display analysis. Treatment of HepG2 cells with TCDD showed a significantly different mRNA expression pattern from the untreated cells in differential display analysis. The differentially displayed bands were isolated and used as probes in dot blot and Northern blot analyses. Of thirty-five isolated differentially displayed bands, only two bands were confirmed as positive in dot blot and Northern blot analyses. The nucleotides sequences of these clones were analyzed and the search of Genebank database revealed that one clone is highly homologous with RanBP2 (Ras-related nuclear protein binding protein2; 92%) and the other is an unknown gene. RanBP2 is a nucleoporin with SUMO E3 ligase activity that functions in both nucleocytoplasmic transport and mitosis and its role as a novel tumor suppressor has been recently proposed. Thus, these results may suggest the clue elucidating the toxic mechanism of TCDD through RanBP2.

• Journal of Animal Reproduction and Biotechnology
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• v.39 no.1
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• pp.48-57
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• 2024

Background: Cadmium (Cd) is toxic heavy metal that accumulates in organisms after passing through their respiratory and digestive tracts. Although several studies have reported the toxic effects of Cd exposure on human health, its role in embryonic development during preimplantation stage remains unclear. We investigated the effects of Cd on porcine embryonic development and elucidated the mechanism. Methods: We cultured parthenogenetic embryos in media treated with 0, 20, 40, or 60 µM Cd for 6 days and evaluated the rates of cleavage and blastocyst formation. To investigate the mechanism of Cd toxicity, we examined intracellular reactive oxygen species (ROS) and glutathione (GSH) levels. Moreover, we examined mitochondrial content, membrane potential, and ROS. Results: Cleavage and blastocyst formation rates began to decrease significantly in the 40 µM Cd group compared with the control. During post-blastulation, development was significantly delayed in the Cd group. Cd exposure significantly decreased cell number and increased apoptosis rate compared with the control. Embryos exposed to Cd had significantly higher ROS and lower GSH levels, as well as lower expression of antioxidant enzymes, compared with the control. Moreover, embryos exposed to Cd exhibited a significant decrease in mitochondrial content, mitochondrial membrane potential, and expression of mitochondrial genes and an increase in mitochondrial ROS compared to the control. Conclusions: We demonstrated that Cd exposure impairs porcine embryonic development by inducing oxidative stress and mitochondrial dysfunction. Our findings provide insights into the toxicity of Cd exposure on mammalian embryonic development and highlight the importance of preventing Cd pollution.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2006.05a
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• pp.91-95
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• 2006

In whole world consciousness of environment maintenance have increased very quickly for the end of the 20th century. To use and disuse toxic substances have been controled at the field of industry. Also the field of lighting source belong to environmental control. And in the future the control will be strong. In radiational mechanism of fluorescence lamp mechanism is the worst environmental problem. In radiational mechanism of fluorescence lamp mercury is the worst environmental problem root. In the mercury free lighting source system the Xe gas lamp is one type. And the Ne:Xe mixing gas lamp improvements firing voltage of Xe gas lamp. Purpose and subject of this study are understand, efficiency, ideal of Ne:Xe plasma which mercury free lamp. Before ICP was designed, basic parameters of plasma, which are electron temperature and electron density, were measured and calculated by Langmuir probe data. Property of electron temperature and electron density were confirmed by changing ratio of Ne:Xe.

• Proceedings of the Korean Society of Propulsion Engineers Conference
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• 2012.05a
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• pp.300-303
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• 2012

Global warming has been a serious problem due to excessive emissions of carbon dioxide from the increase of energy consumption. The present study investigates an energy generation mechanism that does not produce carbon dioxide and oxides of nitrogen. A reaction mechanism including sodium borohydride and hydrogen peroxide has been introduced and as a result, thermal energy can be generated from combustion of hydrogen with oxygen. Sodium borohydride dissolved in water reacting with liquid hydrogen peroxide may reveal maximum adiabatic reaction temperature of 1795 K at a mixture ratio of 0.89.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.16 no.3
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• pp.315-320
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• 1994

General anesthesia is necessary to operation in dept. of oral and maxillofacial surgery. Halothane is one of the most commonly used anesthetic agent for general anesthesia because of its property of nonexplosive, inexpensive, strong activeness and chemical stability. Halothane is fluorinated hydrocarbone anesthetic agent and structurally similiar to chloroform. On the contrary halothane has been reported to result in severe hepaitc necrosis in a small number of individuals. Although the mechanism of halothane induced toxic hapatitis is unclear, it appears to be closely related to reducting metabolite, reactant intermediate product, immune reaction, hypersensitivity and so on. This is a case report of 27 years old male patient occured halothane induced hepatitis following after operation of mandible fracture.