• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2002.11a
• /
• pp.180-180
• /
• 2002

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2003.05a
• /
• pp.68-69
• /
• 2003

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2003.10a
• /
• pp.138-138
• /
• 2003

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2004.05a
• /
• pp.117-117
• /
• 2004

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2004.05a
• /
• pp.140-140
• /
• 2004

• Journal of Microbiology and Biotechnology
• /
• v.14 no.2
• /
• pp.268-275
• /
• 2004

To investigate the potential application of the single-cell gel electrophoresis (SCGE) assay to carp as an aquatic pollution monitoring technique, gill, liver, and blood cells were isolated from carp exposed to a direct-acting mutagen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), or indirect mutagen, $benzo[\alpha]pyrene$ $(B[\alpha]P)$, then the DNA strand breakage was analyzed using the assay. Based on testing 5 different cell isolation methods and 6 electrophoretic conditions, the optimized assay conditions were found to be cell isolation by filter pressing and electrophoresis at a lower voltage and longer running time (at 0.4 V/cm for 40 min). In preliminary experiments, gill and liver cells isolated from carp exposed to MNNG in vitro exhibited DNA damage signals even with 0.5 ppb exposure, which is a much higher dose than previously reported. In the gill cells isolated from carp exposed to 0.01-0.5 ppm MNNG in vivo, significant dose-and time-dependent increases were observed in the tail for 4 days. As such, the linear correlation between the relative damage index (RDI) values and time for each dose based on the initial 48-h exposure appeared to provide effective criteria for the genotoxicity monitoring of direct-acting mutagenic pollution. In contrast, the in vivo exposure of carp to 0.25-1.0 ppm of $B[\alpha]P$ for 7 days resulted in dose-and time-dependent responses in the liver cells, in which 24-h delayed responses for metabolizing activation and gradual repair after 48 h were also observed. Thus, the negative-sloped linear correlation between the RDI and time at each dose based on the initial 48 h appeared to provide more effective criteria for the genotoxicity monitoring of indirect mutagenic pollution.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.05a
• /
• pp.138-138
• /
• 2001

The purpose of the present studies was to investigate the effects of subchronic paternal treatment of cyclophosphamide (CP) and acrolein on male fertility and early embryonic development. Two approaches were pursued. The first was to perform in vivo test for observing the adverse effects of CP and acrolein on the function og male reproductive system and pregnancy outcome.(omitted)

• Toxicological Research
• /
• v.21 no.4
• /
• pp.333-338
• /
• 2005

Many of thyroid hormones disrupting chemicals induce effects via interaction with thyroid hormone and retinoic acid receptors and responsive elements intrinsic in target cells. We studied thyroid hormones disrupting effects of food additives and contaminants including BHA, BHT, ethoxyquin, propionic acid, sorbic acid, benzoic acid, CPM, aflatoxin B1, cadmium chloride, genistein, TCDD, PCBs and TDBE in recombinant HeLa cells containing plasmid construct for thyroxin responsive elements. The limit of response of the recombinant cells to T3 and T4 was $1\times10^{-12}\;M$. BHA. genistein, cadmium and TBDE were interacted with thyroid receptors with dose-responsive pattern. In addition, BHA, BHT, ethoxyquin, propionic acid, benzoic acid, sorbic acid, and TBDE showed synergism while cadmium chloride antagonism for T3-induced activity. This study elucidates that recombinant HeLa cell is sensitive and high-throughput system for the detection of chemicals that induce thyroid hormonal disruption via thyroid hormone receptors and responsive elements. Also this study raised suspect of BHA. BHT, ethoxyquin, propionic acid, benzoic acid, sorbic acid, TBDE, genisteine and cadmium chloride as thyroid hormonal system disruptors.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.05a
• /
• pp.73-74
• /
• 2003

Familial form of Alzheimer's disease (FAD) is caused by mutations in presenilin-1 and presenilin-2 (PS2). PS1 and PS2 mutation are known to similar effects on the production of amyloid $\beta$ peptide (A$\beta$) and cause of cell death in the Alzheimer's brain. The importance of the alternation of calcium homeostasis in the neuronal cell death by PS1 mutation in a variety of experimental system has been demonstrated. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.10a
• /
• pp.98-98
• /
• 2001

Antimutagenic effect of red pepper powder (RPP) produced in Korea depending on the varieties and producing districts were studied against Ν-methyl-Ν'-nitro-Ν-nitrosoguanidine (MNNG) in Ames test and SOS chromotest. The antimutagenic activities of green pepper, red pepper and different parts of dried red pepper were also evaluated in the same experimental systems.(omitted)