• 한국독성학회:학술대회논문집
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• 한국독성학회 2005년도 추계학술대회
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• pp.114-123
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• 2005

• 한국환경과학회:학술대회논문집
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• 한국환경과학회 1994년도 가을 학술발표회 초록집
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• pp.7-7
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• 1994

• 월간산업보건
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• 통권108호
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• pp.15-16
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• 1997

• Toxicological Research
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• 제17권
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• pp.205-210
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• 2001

One of the major focuses and perhaps the greatest challenges during the past decade in the discipline of immunotoxicology has been the elucidation of the molecular mechanisms responsible for immunotoxicity by specific agents. Much is currently understood about the basic underlying intracellular processes that control leukocyte effector function. This fundamental information in cell biology can now be applied toward developing systematic approaches, through the application of cell and molecular biology techniques, to identify the intracellular targets and processes disrupted by immunotoxicants. The objective of this paper is two fold. First to discuss fundamental principles of experimental design aimed at elucidation of cellular mechanisms in immunotoxicology; and second to discuss the application of molecular biology techniques in characterizing the mechanism of TCDD-induced B cell dysfunction as a working example.

• 자연과학논문집
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• 제16권1호
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• pp.129-141
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• 2005

The equilibrium geometry, adiabatic electron affinity, harmonic vibrational frequencies, and infrared intensities of 1,4,6,9-Tetra chlorinated dibenzo-$\rho$-dioxin anion have been studied using B3LYP method. The local minimum conformation is found to be twisted form with $D_2$ symmetry. The predicted adiabatic electron affinity is 0.54 eV. The predicted inversion barrier between twisted and planar conformers was 0.9 kcal/mol, thus we expect that experimentally observed structure seems to be planar. the characteristic IR band of 1,4,6,9-TCDD anion appears at 1510 $cm^4$, which is a benzene ring skeleton vibration mode related with CaCb and C2C3 bond. this characteristic band could be sued for identication of 1,4,6,9-TCDD anion.

• Archives of Pharmacal Research
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• 제14권2호
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• pp.130-136
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• 1991

Nicotine (100 .mu. M) was incubated with microsomes (1 mg/ml) prepared from New Zealand White rabbits. On the basis of microsomal weight, the rate of nicotine oxidation were calculated on the basis of cytochrome P-450 concentration, the specific activity of the metabolic oxidation catalyzed by lung was approximately 4 times greater than liver (6.4 vs 1, 65 nmoles nicotine oxidized. nmole cytochrome $P-450^{-1}\;min{-1})$. These studies employed several methods of altering activities of specific isozymes present in pulmonary microsomes, including the use of the isozyme2 and 6 specific inhibitor $\alpha$-methylbenzyl ABT, metabolite inhibitors, norbenzphetamine and N-hydroxyamphetamine. TCDD induction and Arochlor 1260 pretreatment. These results support the conclusion that nicotine metabolism by rabbit lung microsomes is mediated primarily by cytochrome P-450 isozyme 2.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2004년도 KSOT/KEMS Fall Annual Meeting
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• pp.138-138
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• 2004

• 한국수의병리학회:학술대회논문집
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• 한국수의병리학회 2003년도 추계학술대회초록집
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• pp.42-42
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• 2003

The contamination of the environment with pollutants is one of the main problems of modern life, and the levels pollution in industrialized regions are giving raise to increased public concern. The mitogen-activated protein kinase (MAP kinase) are playa pivotal role in the regulation of important cellular functions by activation of specific signal transduction pathways from cell the surface to the nuclei. Three major subgroups of MAP kinases have been identified, and these comprise the extracellular signal-regulated kinase (ERK), the c-Jun amino-terminal kinase (JNK), and the p38 MAP kinases [1-3]. Herein, we investigated the effect of regulation of phospho-JNK (p-JNK), phospho-p38 (p-p38) and phospho-ERK (p-ERK) by TCDD. (omitted)

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2003년도 추계국제학술대회
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• pp.9-9
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• 2003

There are growing concerns about human health effects of dioxin and dioxin like compounds such as polychlorinated dibenzo-p-dioxins (PCDDS), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs), Earlier studies recognized that 2,3,7,8-tetrachloro dibenzo-p-dioxin (TCDD) and structually related dioxin like compounds invoke a number of common toxic responses that are mediated through a high-affinity cytosolic receptor protein, the AhR. Based on studies that Indicate th pivotal role of AhR in mediating most, if not all, of the dioxin toxicity, TCDD equivalency factor (TEF) approach was developed. This approach allowed the expression of toxic potential of a complex mixture as one integrated parameter, the toxic equivalency (TEQ) value.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.186-186
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• 2001

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxin that activates the aryl hydrocarbon receptor (AhR) and disrupts multiple endocrine signaling pathways by enhancing ligand metabolism, altering hormone synthesis, down regulating receptor levels, and interfering with gene transcription. And TCDD-mediated gene transactivation via the AhR has been shown to be dependent upon estrogen receptor (ER) expression in human breast cancer cells.(omitted)