• Toxicological Research
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• v.13 no.4
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• pp.409-415
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• 1997

The influences of dietary supplement of citron tea on the hepatocellular chemical carcinogenesis have been studied by examining placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of total cytochrome P450, thiobarbituric acid reactive substances(TBARS) and glucose 6-phosphatase(G6Pase) in hepatic microsome and glutathione S-transferase(GST) activity. Weaning Sprague-Dawley male rats were fed AIN76 diet with or without citron tea supplement. Rats of CTR and CTR+ groups were fed diet without citron tea supplement while CDI and CDI+ groups were fed diet with citron tea supplement for the entire experimental period(13 weeks). Rats of CDP and CDP+ groups were fed diet without citron tea supplement for the first 7 weeks and swiched to citron tea containing diet for the last 6 weeks of experimental period. CTR+, CDI+ and CDP+ groups were carcinogen treated group. Diethylnitrosamine(DEN) was used as a carcinogen initiator and injected to the rats of carcinogen treated groups as a single dose of 200 mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acethylaminofiuorene(AAF) was used as a carcinogen promoter and supplied in the diets of carcinogen treated rats as 0.02% content for the last 6 weeks starting from 2 weeks after DEN injection. Rats were sacrificed after 13 weeks of feeding. Liver/body weight ratio and GST activities were increased by carcinogen treatment. However, they were not changed by citron tea supplement. Total cytochrome P450 contents were not changed by carcinogen treatment or citron tea supplement. TBARS contents of carcinogen treated rats showed tendency to decrease by citron tea supplement. G6Pase activity decreased by carcinogen treatment and citron tea supplement. The area of GST-P positive foci detected in carcinogen treated rats were decreased by citron tea supplement and not affected by the timing and the duration of citron tea supplement. These results suggest that citron tea has suppressive effects on hepatocellular chemical carcinogenesis probably through antioxidant compounds by decreasing TBARS contents.

• Toxicological Research
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• v.34 no.4
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• pp.311-324
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• 2018

Arsenic is one of the most toxic environmental toxicants. More than 150 million people worldwide are exposed to arsenic through ground water contamination. It is an exclusive human carcinogen. Although the hallmarks of arsenic toxicity are skin lesions and skin cancers, arsenic can also induce cancers in the lung, liver, kidney, urinary bladder, and other internal organs. Arsenic is a non-mutagenic compound but can induce significant cytogenetic damage as measured by chromosomal aberrations, sister chromatid exchanges, and micronuclei formation in human systems. These genotoxic end points are extensively used to predict genotoxic potentials of different environmental chemicals, drugs, pesticides, and insecticides. These cytogenetic end points are also used for evaluating cancer risk. Here, by critically reviewing and analyzing the existing literature, we conclude that inorganic arsenic is a genotoxic carcinogen.

• Journal of the Korea Safety Management & Science
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• v.12 no.3
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• pp.107-119
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• 2010

The aim of this study was to compare the carcinogen classification systems of developed countries or global organizations with domestic system under Industrial Safety and Health Act (ISHA). We selected the representative institutions which had carcinogen classification system such as International Agency for Research on Cancer (IARC), National Toxicological Program (NTP), Environmental Protection Agency (US-EPA), American Conference of Governmental Industrial Hygienists (ACGIH), and European Union (EU). We collected the carcinogen lists issued by 5 institutions, and merged by CAS number of each chemical with Microsoft Access 7.0. We found that confirmed human carcinogens, probable human carcinogens and possible human carcinogens were 34, 179, and 252, respectively. All of the institutions classified chemicals as 2 (NTP), 3 (EU) or 5 (IARC, ACGIH, US-EPA) categories based on the weight of scientific evidences for carcinogenicity and periodically updated the carcinogen list by regular procedure. However, a total of 90 chemicals could be classified as carcinogen under ISHA in Korea. There was no procedure or system which periodically update the carcinogen lists. In addition, the status of carcinogen classification according to regulation was confused. In conclusion, these findings suggest that the carcinogen classification and management system should be amended by consideration of systems of advanced institutions and the domestic regulation system.

• Molecular & Cellular Toxicology
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• v.1 no.2
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• pp.106-110
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• 2005

N-ethyl-N-nitrosourea (ENU), which is a toxin and a carcinogen, as well as a mutagen, has a variety of effects on mice. ENU induces point mutation in male germ cell. Number of mutant animals are developed with ENU treatment. However, potentiality ot ENU as a carcinogen is not fully understood, even though, mutagenicity of ENU is broadly studied, In the present study, the gene expression profiling and histopathological investigation of ENU treated mouse's liver and brain were investigated. Also, the expression patterns of cancer related genes in ENU-treated mouse were analyzed.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.21 no.4
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• pp.227-235
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• 2011

The objective of this study was to analyze 157 processes of 145 industries that exceeded Korean Occupational Exposure Limits (KOEL) for carcinogen during the 11 year period from 1999 to 2009. The data included number of industry and workers exposed, type of carcinogen and their exceeded ratio, type and size of industry in each year. These data were collected by 46 regional employment & labor offices in Korea using work environment monitoring reports. The result showed that, in each year, about 10 industries exceed their carcinogen exposure limit. The most common carcinogen exceeding KOEL were found to be formaldehyde, benzene, ethylene oxide and chromium VI. The carcinogen with the highest level of over-exposure were in the order of formaldehyde, benzene, ethylene oxide and asbestos. Fabricated metal product manufacturing industry were found to be most vulnerable against carcinogen with 11.1% of them exceeding carcinogen KOEL followed by electronic components manufacturing industry (8.3%), chemical products manufacturing industry (6.3%), and electrical equipments manufacturing industry (4.9%). The industry employing less than 50 workers had the highest percentage of exceeding carcinogen KOEL with 52.8%. The result also showed that strengthening KOEL for benzene and asbestos helped reduce the level of carcinogen over-exposure. Based on these results, strengthening the KOEL or new regulation turned out to help reduce the carcinogen over-exposure level. Benzene, ethylene oxide and chromium VI were the most frequently over-exposed carcinogen with the highest level. Therefore, these chemicals need to be regulated with a highest priority to improve the workplace environment. The results also show that the small-sized industries employing less than 50 workers was the most vulnerable against carcinogen exposures. Therefore, more government support are needed for these small-sized industries to help them to improve their workplace environment.

• Journal of Environmental Health Sciences
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• v.46 no.2
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• pp.159-169
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• 2020

Objectives: The purpose of this study was to investigate changes among the nine kinds of reduction chemical substances in Korea over the period of 2008-2017. We will define basic data for improving the management methods for reducing chemical substances. Methods: A survey of hazardous pollutant emissions for 2008-2017 was conducted through the pollutant Release and Transfer Register homepage. Nine kinds of designated reduction chemical substances (Benzene, Vinyl chloride, Trichloro ethylene, 1,3-butadiene, Dichloro methane, Tetrachloro ethylene, N,N-dimethylformamide, Acrylo nitrile, and Chloroform) provided the study subjects. The emission of hazardous chemicals and health effects used the National Health Statistics and Integrated Chemicals Information System (ICIS) as a reference. Results: Hazardous pollutant emissions increased by 1.2 times over the past decade, and nine types of reduction chemical substances increased by 1.6 times. By region, the emissions of reduction chemical substances over the last 10 years were in the order of Chungbuk, Gyeonggi, and Gyeongbuk. Emissions of Dichloro methane was the highest in Chungbuk and Gyeongbuk. N,N-dimethylformamide was the highest in Gyeonggi. Carcinogen pollutant emissions showed a tendency to increase continuously. In addition, group 1 carcinogen emissions showed a tendency to decrease. Conclusion: In the last decade, the amount of hazardous chemical emissions has been continuously increasing. Hazardous chemical emissions require facility improvement for continuous emissions reduction. More research on reduction of emissions is needed.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.24-25
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• 2003

Genotoxicity plays an important role for the safety evaluation of chemicals. When the carcinogenicity is evident on a chemical, the threshold can be estimated only when genotoxic mechanism does not operate for carcinogenesis otherwise threshold cannot be set. Without genotoxic mechanism- non-genotoxic carcinogen-threshold can be estimated but with genotoxic mechanism-genotoxic- carcinogen-it cannot be estimated.(omitted)

• Korean Journal of Community Nutrition
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• v.2 no.5
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• pp.735-744
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• 1997

The effect of green tea drinking on the hepatocellular chemical cacinogenesis have been studied. Placental glutathione S-transferase(GST-P) positive foci area in a liver tissue, contents of thiobarbituric acid reactive substances(TBARS), total cytochrome P450 and glucose 6-phospphatase(G6P) activity in hepatic microsomes were investigated. Weaning Sprague-Dawley male rats were fed AIN-76A diet with deionized water or green tea infusion, Rats of CTR and CTR+ groups were provided deionized water while GTI and GTI+ groups were provided green tea instead of deionized water for the entire experimental period of 13weeks. Rats of GTP and GTP + groups had deionized water for the first 6 weeks and switched to green tea for the last 7weeks of the experimental period. CTR+, GTI +, and GTP + groups were carcinogen treated groups, Diethylnitrosamine(DEN) was injected as a single dose of 200mg/kg body weight intraperitoneally after 4 weeks of feeding. 2-Acetyla-minofluorene(AAF) was used as a carcinogen proliferater and suppled in the diets of carcinogen treated rats as 0.02% content for the last 6weeks starting from 2weeks after DEN injection. Rats were sacrificed after 13week weeks of feeding. The area and number of GST-P positive foci detected in carcinogen treated rats were decreased by green tea ingestion but when timing and duration of green tea ingestion was delayed after promotion period as in GTP + group, GST-P positive foci were not decreased as much as in GTI+ group. TBARS contents of carcinogen treated rats decreased by 13weeks of green tea ingestion but GTP groups did not show statiscally significant differences. G6P activities tended to decrease by carcinogen treatment but changes were not statiscally significant by green tea ingestion. Total cytochrome P450 contents were increased by carcinogen treatment. Thirteen weeks of green tea ingestion (GTI) also increased to total cytochrome P450 contents while 7weeks of green tea ingestion(GTP) did show any effects. These results suggest that green tea has suppressive effects on hepatocellular chemical carcinogenesis probably through the activities of antioxidant compounds. (Korean J Community utrition 2(5) : 735∼744, 1997)

• Journal of Environmental Health Sciences
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• v.44 no.2
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• pp.160-168
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• 2018

Objectives: The purposes of the study were to investigate hazardous pollutant emissions changes among group 1 carcinogens. The emissions characteristics were compared with national cancer registration statistics. Methods: A survey of group 1 carcinogen hazardous pollutant emissions (trichloroethylene, benzene, vinyl chloride, formaldehyde, 1,3-butadiene, ethylene oxide, chromium and its compounds, 3,3'-dichloro-4,4-diaminodiphenylmethane, chloromethyl methyl ether, arsenic and its compounds, cadmium and its compounds, o-toluidine) was conducted through a homepage for 2001-2015. The emission of hazardous chemicals and the cancer trend analysis for 2001-2015 were performed using the Korean statistical information service through its homepage as a reference. Results: Emissions of more than 95% of the substances listed as group 1 carcinogens over the last five years were made up of trichloroethylene, benzene, vinyl chloride, formaldehyde, 1,3-butadiene, and ethylene oxide. As a result of the comparison of emission results and cancer incidence rates, carcinogen pollutant emissions showed a tendency to decrease continuously. In addition, the incidence of cancer tended to increase, but showed a tendency to decrease from 2012. Conclusion: The results indicate hazardous pollutant emissions have continued to increase. However, no association between emissions and health effects was shown and more research is needed.

• Preventive Nutrition and Food Science
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• v.7 no.1
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• pp.67-71
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• 2002

Capsaicin (trans-8-methyl-N-vanillyl-6-nonenarnide), a major pungent component of hot pepper, is known to exert antioxidative properties. In this study, we investigated the protective effects of capsaicin against chemical carcinogen-induced oxidative damage in rats. Male Sprague Dawley rats weighting 230~250 g were treated with chemical carcinogens such as 2-nitropropane (2NP) or n-methyl-N'-nitro-N-nitrosoguanidine (MNNG) after (or before) the administration of capsaicin at doses of 0.5, 1,5 mg/kg. The level of lipid peroxidation in rat liver was estimated by measuring the amounts of thiobarbituric acid reactive substances. The degree of oxidative DNA damage was evacuated by measuring a DNA adduct, 8-hydroxydeoxyguanosine (8-OHdG), in urine. Antioxidative activities of capsaicin and its metabolites in vitro were determined by the measurement of DPPH (1,1-diphenyl-2-picrylhydrazyl), a radical quencher. Significant inhibition of 2-NP induced lipid peroxidation was observed in the liver of the rat when treated with capsaicin. MNNG-induced urinary excretion of 8-OHdG was decreased by capsaicin treatment. Capsaicin and its metabolites inhibited net only the formation of free radicals, but also lipid peroxidation in vitro. Our results show that capsaicin may function as a free radical scavenger against chemical carcinogen-induced oxidative cellular damage in vivo. The observed antioxidative activities of capsaicin may play an important role in the process of chemoprevention.