• Proceedings of the Korean Society of Life Science Conference
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• 2002.09a
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• pp.67-68
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• 2002

• Proceedings of the Korean Society of Life Science Conference
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• 2003.05a
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• pp.19-22
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• 2003

• Proceedings of the Korean Society of Life Science Conference
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• 2002.03a
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• pp.78-78
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• 2002

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.197.2-197
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• 1999

No Abstract, See Full Text

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.196.2-196.2
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• 2000

• Archives of Pharmacal Research
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• v.19 no.4
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• pp.251-257
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• 1996

The detection of many synthetic chemicals used in industry that may pose a genetic hazard in our environment is subject of great concern at present. In this respect, the genetic toxicity of fenpropathrin ((RS)-.alpha.-cyano-3-phenoxybenzyl-2,2,3,3-tetramethyl cyclopropane carboxylate, CAS No.:39514-41-8), a pyrethroid insecticide, was evaluated in bacterial gene mutation system, chromosome aberration in mammalian cell system and in vivo micronucleus assay with rodents. In bacterial gene mutation assay, no mutagenicity of fenpropathrin (62-$5000\mug/plate$) was observed in Salmonella typhimurium TA 98, 100, 1535 and 1537 both in the absence and in the presence of S-9 metabolic activaton system. In mammalian cell system using chinese hamster lung fibroblast, no clastogenicity of fenpropathrin was also observed both in the absence and in the presence of metabolic activation system in the concentration range of $7-28\mug/ml$. And also, in vivo micronucleus assay using mouse bone marrow cells, fenpropathrin also revealed no mutagenic potential in the dose range of 27-105 mg/kg body weight of fenpropathrin (i.p.). Consequently, no mutagenic potential of fenpropathrin was observed in vitro bacterial, mammalian mutagenicity systems and in vivo micronucleus assay in the dose ranges used in this experiment.

• Molecules and Cells
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• v.20 no.1
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• pp.83-89
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• 2005

HtrA2/Omi is a mammalian mitochondrial serine protease homologous to the E. coli HtrA/DegP gene products. Recently, HtrA2/Omi was found to have a dual role in mammalian cells, acting as an apoptosis-inducing protein and being involved in maintenance of mitochondrial homeostasis. By screening a human brain cDNA library with $A{\beta}$ peptide as bait in a yeast two-hybrid system, we identified HtrA2/Omi as a binding partner of $A{\beta}$ peptide. The interaction between $A{\beta}$ peptide and HtrA2/Omi was confirmed by an immunoblot binding assay. The possible involvement of HtrA2/Omi in $A{\beta}$ peptide metabolism was investigated. In vitro peptide cleavage assays showed that HtrA2/Omi did not directly promote the production of $A{\beta}$ peptide at the ${\beta}/{\gamma}$-secretase level, or the degradation of $A{\beta}$ peptide. However, overexpression of HtrA2/Omi in K269 cells decreased the production of $A{\beta}40$ and $A{\beta}42$ by up to 30%. These results rule out the involvement of HtrA2/Omi in the etiology of Alzheimer's disease. However, the fact that overexpression of HtrA2/Omi reduces the generation of $A{\beta}40$ and $A{\beta}42$ suggests that it may play some positive role in mammalian cells.

• Environmental Mutagens and Carcinogens
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• v.21 no.2
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• pp.99-105
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• 2001

Sophoricoside was isolated as the inhibitor of IL-5 bioactivity from Sophora japonica (Leguminosae). It has been reported to has an anti-inflammatory effect on rat paw edema model. To develope as an anti-allergic drug, genotoxicity of sophoricoside was investigated in bacterial and mammalian cell system such as Ames bacterial reversion test, chromosomal aberration assay and single cell gel electrophoresis (Comet) assay. As results, in the range of 1,250~40 $\mu\textrm{g}$/plate sophoricoside concentrations was not shown significant mutagenic effects in Salmonella typhimurium TA 98, TA 100, TA 1535 and TA 1537 strains in Ames test. The 80% cell growth inhibition concentration (IC/SUB 80/) of sophoricoside was determined as above 5,000 $\mu\textrm{g}$/$m\ell$ in Chinese hamster lung (CHL) fibroblast cell and L5178Y mouse lymphoma cell line for the chromosomal aberration and comet assay, respectively. Sophoricoside was not induced chromosomal aberration in CHL fibroblast cell at concentrations of 700, 350 and 175 $\mu\textrm{g}$/$m\ell$ or 600, 300 and 150 $\mu\textrm{g}$/$m\ell$ in the absence or presence of S-9 metabolic activation system, respectively. Also, in the comet assay, the induction of DNA damage was not observed in L5178Y mouse lymphoma cell line both in the absence or presence of S-9 metabolic activation system. From these results, no genotoxic effects of sophoricoside were observed in bacterial and mammalian cell systems used in these experiments.

• KSBB Journal
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• v.4 no.1
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• pp.34-39
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• 1989

Growth kinetics of mammalian cell, Chinese Hamster Ovalry(CHO) was investigated to effectively produce pharmaceutically important Erythropoeitin under perfusion chemostat conditions. Perfusion rate, D is correlated with total viable is to be an essential factor in controlling growth kinetic parameters under this kind of operations. It is also found that the measurement of oxygen uptake rates is a relatively accurate method to understand cell growth, in case that the traditional cell count method is no longer useful due to heavy cell clumpings. True growth yield, Ymax and maintenance coefficient, me associated with mammalian cell growth were estimated as $2.86{\times}10^8$ cells/ g of glucose and 0.0063 g of glucose/ cells/ hr, respectively.

• BMB Reports
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• v.28 no.3
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• pp.221-226
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• 1995

Dopamine mediates inhibitory responses in Helix aspersa neurons from the right parietal lobe ("F-lobe") of the circumoesophageal ganglia. The effects appeared as a dose-dependent hyperpolarization of the plasma membrane and a decrease in the occurrence of spontaneous action potentials. The average hyperpolarization with 5 ${\mu}m$ dopamine was -12 mV (${\pm}1.5$mV, S.D., n=12). Dopamine also modulated the currents 'responsible for shaping the action potentials in these neurons. When dopamine was added and action potentials were triggered by an injection of current, the initial depolarization was slowed, the amplitude and the duration of action potentials were decreased, and the after-hyperpolarization was more pronounced. The amplitude and the duration of action potential were reduced about 15 mV and about 13% by 5 ${\mu}m$ dopamine, respectively. The effects of dopamine on the resting membrane potentials and the action potentials of Helix neurons were dose-dependent in the concentration range 0.1 ${\mu}m$ to 50 ${\mu}m$. In order to show 1) that the effects of dopamine were mediated by dopamine receptors rather than by direct action on ionic channels and 2) which type of dopamine receptor might be responsible for the various effects, we assayed the ability of mammalian dopamine receptor antagonists, SCH-23390 (antagonist of D1 receptor) and spiperone (antagonist of D2 receptor), to block the dopamine-dependent changes. The D1 and D2 antagonists partially inhibited the dopamine-dependent hyperpolarization and the decrease in action potential amplitude. They both completely blocked the decrease in action potential duration and the increase in action potential after-hyperpolarization. The dopamine-induced slowdown of the depolarization in the initial phase of the action potentials was less effected by SCH-23390 and spiperone. From the results we suggest 1) that Helix F-lobe neurons may have a single type of dopamine receptor that binds both SCH-23390 and spiperone and 2) that the dopamine receptor of Helix F-lobe neurons may be homologous with and primitive to the family of mammalian dopamine receptors.