• Journal of Environmental Health Sciences
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• v.36 no.4
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• pp.294-305
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• 2010

This study estimated the health risk of heavy metals in particulate matter $(PM)_{2.5}$ in a Gwangyang industrial complex. The $PM_{2.5}$ containing heavy metal was collected from January to November, 2008 using a denuder air sampler and by IC (Ion Chromatograph). The risk assessment was performed in a four-step process; hazard identification, exposure assessment, dose-response assessment and risk characterization. In the hazard identification process, $Cr^{6+}$, Ni, As, and Pb were categorized as human carcinogens and probable human carcinogens, while Ti, Mn, Se, P, $Cr^{3+}$, Cu, and Zn were not classified as human carcinogens. It was found that the excess cancer risk by Central Tendency Exposure (CTE) of $Cr^{6+}$ and As in $PM_{2.5}$ was > $10^{-6}$, and the total excess cancer risk posed by carcinogen heavy metals in $PM_{2.5}$ was > $10^{-6}$. It was also determined that the total hazard index by CTE of non-carcinogen heavy metals in $PM_{2.5}$ was <1. Taken together, these results indicate a high cancer risk associated whit inhalation of heavy metal-containing$PM_{2.5}$ in industrial areas.

• 대한약리학회:학술대회논문집
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• 2006.11a
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• pp.69.2-69.2
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• 2006

• Journal of Environmental Impact Assessment
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• v.8 no.2
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• pp.1-8
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• 1999

The research centers on the concentration profile and risk assessment of toxic metals for ambient air in Taejon industrial complex. Airborne concentrations of each toxic metal for risk assessment were obtained from 2-year sampling by high volume air sampler and analysis by ICP-MS and ICP-AES in the complex. The long-term arithmetic mean of human carcinogen, arsenic, hexavalent chromium and nickel subsulfide was 5.53, 2.16 and $3.46ng/m^3$ while the mean of probable human carcinogen, beryllium, cadmium and lead was 0.08, 2.35, $293.29ng/m^3$, respectively. And the long-term arithmetic mean concentration of non-carcinogenic metal, manganese was $55.91ng/m^3$. The point risk estimate for the inhalation of carcinogenic metals was $3.6{\times}10^{-5}$, which was higher than a risk standard of $10^{-5}$. About 75% of the cancer risk was to the inhalation of human carcinogen, arsenic. Thus, it is necessary to properly manage arsenic risk in Taejon industrial complex. The point hazard index by the inhalation of manganese was 1.1. Therefore, an investigation into Taejon industrial complex is needed to obtain more fine long-term concentration data for airborne non-carcinogenic metals including manganese.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05b
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• pp.1-19
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• 2002

It is well established that the initiating event in chemical carcinogenesis is the binding of reactive carcinogens to DNA. Thus, a number of analytic methods have been developed for determining levels of carcinogen-DNA adducts in humans as a marker of individual exposure and, potentially, of risk for cancer development. In addition, reactive carcinogens also bind to protein suggesting protein adducts can be used as a surrogate for DNA adducts in some situations. We have developed monoclonal and polyclonal antibodies to carcinogen-DNA and protein adductis and highly sensitive ELISA and immunohistochemical assays for determining levels of adducts in human tissues. These studies have demonstrated higher levels of adducts in those with higher exposure as a result of workplace, dietary, chemotherapy, environmental of lifestyle (smoking) exposures. Elevated levels of adducts have been found in lung and liver cancer cases compared to controls. We have also used DNA adducts to determine efficacy of an antiosidant vitamin intervention. DNA adduct studies have demonstrated very different levels of damage in those with similar exposure levels. These interindividual differences are likely the result genetic differences in capacity to activate carcinogens, detoxify reactive intermediates and repair DNA adducts once formed. We are currently investigating the relationship between polymorphisms in a number of these genes to determine their relationship to adduct levels as well as their ability to confer increased risk for cancer development. The ability to identify high risk individuals will allow the targeting of screening and preventive strategies to those most likely to benfit.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.7
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• pp.4235-4238
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• 2013

Glucoraphanin is the main glucosinolate found in broccoli and other cruciferous vegetables (Brassicaceae). The objective of the study was to evaluate whether glucoraphanin and its breakdown product sulforaphane, are potent modulators of various phase I and phase II enzymes involved in carcinogen-metabolising enzyme systems in vitro. The glucosinolate glucoraphanin was isolated from cruciferous vegetables and exposed to human hepatoma cell line HepG2 at various concentrations (0-25 ${\mu}M$) for 24 hours. Glucoraphanin at higher concentration (25 ${\mu}M$) decreased dealkylation of methoxyresorufin, a marker for cytochrome P4501 activity; supplementation of the incubation medium with myrosinase (0.018 U), the enzyme that converts glucosinolate to its corresponding isothiocyanate, showed minimal induction in this enzyme activity at concentration 10 ${\mu}M$. Quinone reductase and glutathione S-transferase activities were unaffected by this glucosinolate; however, supplementation of the incubation medium with myrosinase elevated quinone reductase activity. It may be inferred that the breakdown product of glucoraphanin, in this case sulforaphane, is superior than its precursor in modulating carcinogen-metabolising enzyme systems in vitro and this is likely to impact on the chemopreventive activity linked to cruciferous vegetable consumption.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2000.09a
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• pp.26-26
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• 2000

The consumption of cruciferous vegetables such as cabbage and broccoli have been shown to have a chemopreventive effect in human and in experimental animals. Indole-3-carbinol (I3C), one component of cruciferous vegetables, has been shown to exert its chemopreventive effect in liver, colon and mammary tissue before or concurrent exposure of carcinogen, but in some reports, there have been several evidence that consumption of I3C after carcinogen treatment induced tumor promotion in some tissues. There have been no reports about the effect of I3C after carcinogen exposure in N-Nitroso-N-methylurea (MNU)-induced mammary tumor model of rats. (omitted)

• Parasites, Hosts and Diseases
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• v.46 no.3
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• pp.127-132
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• 2008

Clonorchis sinensis is one of the most prevalent parasitic helminths in Korea. Although cholangiocarcinoma can be induced by C. sinensis infection, the underlying mechanism is not clearly understood. To assess the role of C. sinensis infection in carcinogenesis, an in vitro system was established using the human epithelial cell line HEK293T. In cells exposed to the excretory/secretory products (ESP) of C. sinensis and the carcinogen dimethylnitrosamine (DMN), cellular proliferation and the proportion of cells in the G2/M phase increased. Moreover, the expression of the cell cycle proteins E2F1, p-pRb, and cyclin B was dramatically increased when ESP and DMN were added together. Similarly, the transcription factor E2F1 showed its highest level of activity when ESP and DMN were added simultaneously. These findings indicate that DMN and ESP synergistically affect the regulation of cell cycle-related proteins. Our results suggest that exposure to C. sinensis and a small amount of a carcinogen such as DMN can promote carcinogenesis in the bile duct epithelium via uncontrolled cellular proliferation and the upregulation of cell cycle-related proteins.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.29-30
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• 2003

The heavy metal cadmium is a xenobiotic toxicant of environmental and occupational concern and it has been classified as a human carcinogen. Inhalation of cadmiumhas been implicated in the development of emphysema and pulmonary fibrosis, but, the detailed mechanism by which cadmium induces adverse biological effects is not yet known.(omitted)

• Korean Journal of Food Science and Technology
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• v.28 no.3
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• pp.421-427
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• 1996

Ethyl carbamate is an animal carcinogen and a suspected human carcinogen found in fermented foods and beverages. For the determination of ethyl carbamate in typical Korean diet, an analytical method was established for the food as complex as Kimchi. Kimchi samples collected from various locations in the country were homogenized and extracted four times with ethyl acelate. Following concentration and reconstitution with water, the extract was loaded onto $C_{18}$ column. Fraction containing ethyl carbamate was eluted with methanol, while most of the red pigment of the sample was retained on the column. The eluent was further purified with alumina, followed by Florisil column. The final eluent was analyzed by gas chromatography mass spectrometry in the selected ion monitoring mode. None of the twenty Kimchi samples showed ethyl carbamate level higher than 4.6 ppb without correction for the recovery. The concentration of ethyl carbamate in Kimchi increased as pH decreased, suggesting fermentation dependent formation of ethyl carbamate.