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Hyo Kyun Chung  (Chung HK) 2 Articles
Peroxiredoxin I and II are Involved in Hydrogen Peroxide Regulation in FRTL-5 Thyroid Cells.
Ho Kim, Tae Hoon Lee, Eun Shin Park, Jae Mi Suh, Soo Jung Park, Hyo Kyun Chung, Hyun Jin Kim, Soo Hong Chae, Do Hee Kim, O Yu Kwon, Young Kun Kim, Min Ho Shong, Heung Kyu Ro
J Korean Endocr Soc. 2000;15(1):55-69.   Published online January 1, 2001
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BACKGROUND
Peroxiredoxins (Prx) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. One mechanism for this action involves modulation of hydrogen peroxide (H2O2)-mediated cellular responses. This report examines the expression of Prx I and Prx II in thyroid cells and their roles in eliminating H2O2 produced in response to TSH. METHODS: The expression of Prx-I and Prx-II were quantiated in FRTL-5 after stimulation with Thyroid stimulating hormone (TSH), Forskolin (FSK), Methimazole (MMI) and hydrogen peroxide (H2O2). Transient transfections were carried out with FRTL-5 cells at 80% confluency and 20microgram of pCRprx I and pCRprx II or equivalent molar amounts of the pCR3.1TM basic vector. Transient transfection used an electroporation technique. Intracellular H2O2 was assayed in FRTL-5 cells with a fluorescent dye, 2', 7'-dichlorofluoresceindiacetate (DCFH-DA). Apoptosis of cells were evaluated by using an detection kit (Promega, Inc., Madison, WI). RESULTS: Prx I and Prx II are constitutively expressed in FRTL-5 thyroid cells. Prx I expression, but not Prx II expression, is stimulated by exposure to TSH and H2O2. In addition, methimazole (MMI) induces a high level of Prx I mRNA and protein in these cells. Overexpression of Prx I and Prx II enhance the elimination of H2O2 produced by TSH in FRTL-5 cells. Treatment with 500microM H2O2 causes apoptosis in FRTL-5 cells as evidenced by standard assays of apoptosis (i.e., terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end-labeling (TUNEL), BAX expression and PARP cleavage. Overexpression of Prx I and Prx II reduces the amount of H2O2-induced apoptosis measured by these assays. CONCLUSION: These results suggest that Prx I and Prx II are involved in the removal of H2O2 in thyroid cells, and can protect these cells from undergoing apoptosis. These proteins are likely to be involved in the normal physiological response to TSH-induced production of H2O2 in thyroid cells.
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A Case of Thyrotoxicosis During Lithium Therapy.
Young Sik Choi, Yo Han Park, Joon Chul Pyun, Dal Soo Park, Chul Hee Lee, Hyo KYun Chung, Hyun Joo Kim, Soo Yeol Ahn, Jin Sook Jun, Yong Chang Oh
J Korean Endocr Soc. 1998;13(4):629-633.   Published online January 1, 2001
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Lithium has been established as a drug useful for the treatment of manic depressive disorder. It is now well recognized that long-term administration of this drug is associated with various antithyroid effects such as goiter, and subclinical and overt hypothyroidism. However, it has been associated less commonly with thyrotoxicosis. Recently we experienced a case of thyroitoxicosis during lithium therapy. A 24-year-old man treated with lithium carbonate 900 mg-1,200 mg/day for manic-depressive illness for four weeks. He then complained of nervousness, palpitation, tremor, heat intolerance, and sweating. Neck pain was not noted. At that time the results of thyroid function test were consistent with hyperthyroidism: T3 568.8 ng/dL, TSH 0.01 mU/mL, FT4 6.0 ng/dL, but 24 hr radioiodine uptake was 0.3%. We suspected this case as lithium induced thyrotoxicosis and discontinued lithium administration. After discontinuation of lithium thyrotoxic symptoms were subsided. One month later, thyroid hormon levels became normalized: T 100.2 ng/dL, TSH 0.06 mU/mL, FT4 0.97 ng/dL and 24hr radioiodine uptake was 16%. We report this case with review of literatures.
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