- Placental Superoxide Dismutase, Genetic Polymorphism, and Neonatal Birth Weight.
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Yun Chul Hong, Kwan Hee Lee, Moon Whan Im, Young Ju Kim, Eun Hee Ha
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J Prev Med Public Health. 2004;37(4):306-311. Published online November 30, 2004
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- BACKGROUND
The roles of antioxidants in the placenta and genetic susceptibility to oxidant chemicals in relation to neonatal birth weight have not been elucidated. We determined whether the level of placental manganese superoxide dismutase (MnSOD) and its genetic polymorphism plays any role in oxidative stress and neonatal birth weight. METHODS: We measured placental MnSOD and determined MnSOD genetic polymorphism among 108 pregnant women who were hospitalized for delivery and their singleton live births in Korea. Main outcome measurements are maternal urinary malondialdehyde (MDA) and birth weight. RESULTS: Maternal urinary concentrations of MDA were significantly associated with neonatal birth weight (P=0.04). The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (P< 0.01). We observed dose-response relationships between placental MnSOD and maternal urinary MDA, and neonatal birth weight after adjusting for maternal weight, height, age, and neonatal sex. After controlling for covariates, MnSOD variant genotype increased maternal urinary MDA concentrations (P< 0.01) and reduced birth weight by 149 gm (P=0.08). CONCLUSIONS: This study demonstrates that the placental level of MnSOD during pregnancy significantly affects fetal growth by reducing oxidative stress, and that genetic polymorphism of MnSOD probably modulate the effects of oxidants on fetal growth.
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- Exposure Assessment of PCDD/Fs and Monitoring of Health Effects on Workers and Residents near the Waste Incinerators in Korea.
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Jong Han Leem, Yun Chul Hong, Kwan Hee Lee, Ho Jang Kwon, Jae Yeon Jang
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Korean J Prev Med. 2003;36(4):314-322.
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- OBJECTIVES
In this study, the exposure status of the hazardous substances from incinerators, such as polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), were studied, and the relationship between the exposure of these hazardous substances and their heath effects on the workers and residents near municipal solid waste (MSW) incinerators and an industrial incinerator investigated. METHODS: Between July 2001 and June 2002, 13 workers at two MSW incinerators, 16 residents from the area around the two MSW incinerators, 6 residents from the control area, and further 10 residents near an industrial incinerator, estimated to emit higher levels of hazardous substances, were interviewed. Information, including sociodemographic information, personal habits, and work history, detailed gynecologic and other medical history were collected through interviews. Blood samples were also collected from 45 subjects, and analyzed for PCDD/DFs, by high resolution gas chromatography - high resolution mass spectrometry, using the US EPA 1613 method. In addition to the questionnaire survey, urinary concentrations of 8-hydroxydeoxyguanosine (8-OH-dG) and malondialdehyde (MDA) were measured as oxidative injury biomarkers. The urinary concentrations of 8-OH-dG were determined by in vitro ELISA, and the MDA by HPLC, using an adduct with thiobarbituric acid. RESULTS: The PCDD/DFs concentrations in the residents near the industrial incinerator were higher than those in the controls, workers and residents near the MSW incinerators. The average TEQ (Toxic Equivalencies) concentrations of the PCDD/DFs in residents near the industrial incinerator were 53.4pg I-TEQs/g lipid. The estimated daily intakes were within the tolerable daily intake range (1-4 pg I-TEQ/Kg bw/day) suggested by WHO (1997) in only 30% to the people near the industrial incinerator. Animal studies have already shown that even a low body burden of PCDD/DFs, such as 10ng TEQ/kg bw, can cause oxidative damage in laboratory animals. Our study also showed that the same body burden of PCDD/DFs can cause oxidative damage to humans. CONCLUSIONS: The exposures to PCDD/DFs and the oxidative stress of residents near the industrial incinerator, were higher than those in the controls, workers and residents near the MSW incinerators. Proper protection strategies against these hazardous chemicals are needed. Because a lower body burden of PCDD/Fs, such as 10ng TEQ/kg bw, can cause oxidative damage, the tolerable daily intake range should be restrictedly limited to 1pg I-TEQ/kg bw/day.
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Summary
- Specimen Storage and Analysis for Genomic Epidemiology.
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Yun Chul Hong, Kwan Hee Lee
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Korean J Prev Med. 2003;36(3):209-212.
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- Because of advances of technologies in the field of genomic epidemiology in the recent years, specimen collection, storage and analysis became an essential part of research methodologies. DNA is now being used in epidemiologic studies to evaluate genetic risk factors and specimens other than the fresh whole blood can be used for PCR. Therefore, All nucleated cells, such as buccal swabs and urine specimens, are suitable for DNA analysis. For an unlimited source of genomic DNA, EBV transformation of lymphocytes can be used for immortalization. However, the type of specimen collected in genomic epidemiologic studies will depend on the study where the epidemiologist play a leading role for the design. We also briefly described various kinds of analysis for SNP that is an essential part of the genomic epidemiology.
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- In Vitro Assessment of Cytotoxicity and Mutagenicity of Rock Wool Fibers.
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Yun Chul Hong, Kwan Hee Lee
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Korean J Prev Med. 1997;30(3):555-566.
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- This study was carried out to evaluate the cytotoxicity of rock wool fibers(RWFs) such as cell division disturbance, chromosomal and DNA damage, and mutagenicity using cultured cells. RWFs were the man made mineral fibers. In order to find the correlation between the cytotoxicity of RWFs and the phagocytic capacity of cells, the phagocytic processes were observed using scanning electron microscope. Cell division disturbance by RWFs was evaluated by the formation of multinucleated giant cells. The chromosomal damage was evaluated by the micronucleus formation. For the evaluation of oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine (8-OH-dG) formation was measured utilizing calf thymus DNA. Mutagenicity was determined by the point mutation of HGPRT and the effect of RWFs on cell transformation was also observed. 1. Compared with the results of chrysotile, RWFs were no or little effect on the cell growth according to the results done by the tests of cell proliferation inhibition and relative plating efficiency. 2. The frequency of multinucleated giant cell formation was increased by the treatment of RWFs and it was dose-dependent. However, the effect of RWFs was weaker than that of chrysotile. 3. The number of micronuclei formed in the RWFs treated cells was between those of cells treated with chrysotile and those of untreated cells. 4. The 2 fold increase in the formation of 8-OH-dG in calf thymus DNA was observed in the cells treated with RWFs in the presence of H2O2. On the other hand, chrysotile had no effect on the 8-OH-dG formation. 5. RWFs had no effect on the HGPRT point mutation and cell transformation. These results showed that RWFs could induce chromosomal damage, cell division disturbance and oxidative DNA damage in the RWFs treated cells.
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Summary
- Repair of Chromate induced DNA-Protein Crosslinks in Rat Lymphocyte.
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Hun Jae Lee, Kwan Hee Lee, Yun Chul Hong
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Korean J Prev Med. 1996;29(3):597-608.
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- Genotoxic agents can induce various DNA lesions. DNA-Protein Crosslinks(DPCs) were known as the important DNA lesions which could impair gene expression because DPCs had a high probability of resisting repair and persisting through cell cycle. This repair resistance of DPCs could have biological significance but had not been evaluated clearly yet. Most of the studies that have evaluated the repair of DPCs only compared the extent of DPCs repair with other DNA lesions. We injected K2CrO4, a genotoxic agent, into Sprague-Dawley rats intraperitoneally(5mg/kg) and isolated blood lymphocytes 12 hours later. These lymphocytes were cultured in the mitogen added growth media and mitogen free media separately. The degree of the repair of DPCs was monitored for 4 days by the K-SDS assay. 4 day later, the amount of DPCs decreased by 4.6% in the mitogen added media but in creased by 10.9% in the mitogen free media. These results showed that DPCs induced by K2CrO4 were not repaired easily and the DPCs were biologically significant DNA lesions. We thought the decrease of DPCs in the mitogen added media was not due to the repair of DPCs, but from the increase of normal cell proliferation. Therefore, it is very important to consider the proliferation of normal cells when estimating the repair of DPCs.
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