• Journal of the Korean Chemical Society
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• v.33 no.6
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• pp.614-622
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• 1989

The electrochemical reduction of ${\alpha},{\beta}$-dibenzyl N-benzylidene L-aspartate in 0.1M LiCl ethanol solution was investigated by direct current (DC), differential pulse (DP) polarography, cyclic voltammetry and controlled potential coulometry(CPC). The irreversible reductive amination of imino group proceeded to form ${\alpha},{\beta}$-dibenyl N-benzyl L-aspartate by CEC or CE electrochemical reaction mechanism at the first reduction step (-0.92 volts vs. Ag-AgCl). The polarographic reduction wave was slightly suppressed due to inhibitory effect of micelle, while the irreversibility was increased according to the increase of Triton X-100 concentration. Upon the basis of product analysis and polarogram interpretation with pH change, possible CE electrode reaction mechanism was suggested.

• Korean Journal of Weed Science
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• v.14 no.1
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• pp.23-27
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• 1994

Nutrient culture study was initiated to examine the selectivity of dithiopyr(S, S-dimethyl 2-difluoromethyl)-4-(2-methylpropyl)-6-(trifluoro methyl)-3, 5-pyridine dicarbothiate) in rice(Oryza sativa L.) and barnyardgrass(Echinochloa crusgalli Beauv.). Absorption and translocation of $^{14}C$-dithiopyr in rice and barnyardgrass were also investigated to determine their selective mechanism. Rice was very tolerant, but barnyardgrass was susceptible to dithiopyr. The absorption of dithiopyr was greater in barnyardgrass than in rice and most of them remained in the roots of both species. Dithiopyr was absorbed by roots and basal shoots of both species. Translocation of dithiopyr was very low but was higher in barnyardgrass than in rice. Therefore, this study suggest that the selectivity of dithiopyr between rice and barnyardgrass may be mainly attributed to the absorption and translocation of dithiopyr in plants.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.63-70
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• 2006

Background: Testosterone is reported to have neuroprotective effect in various neurological diseases. Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The Cu/Zn-superoxide dismutase (SOD1) mutations has been implicated in selective motor neuron death of amyotrophic lateral sclerosis (ALS) and it is said to play an important role in NO-mediated motor neuron death. However, neuroprotective effect of testosterone on motor neuron exposed to NO has rarely been studied. Methods: Motor neuron-neuroblastoma hybrid cells expressing wild-type or mutant (G93A or A4V) SOD gene were treated with $200{\mu}M$ S-nitrosoglutathione. After 24 hr, cell viability was measured by MTT assay. To see the neuroprotective effect of testosterone, pretreatment with 1 nM testosterone was done 1 hr before S-nitroglutathione treatment. To study the mechanism of protective effect, $20{\mu}M$ flutamide (androgen receptor antagonist) was also pretreated with testosterone 1 hr before S-nitroglutathione treatment. Results: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was somewhat different in each cell line. 1 nM testosterone showed neuroprotective effect in G93A and wild-type cell line. In A4V cell line, testosterone did not showed neuroprotective effect. The neuroprotective effect of testosterone was reversed by $20{\mu}M$ flutamide. Conclusions: These results indicate that testosterone induces neuroprotection in NO-mediated motor neuron death directly through the androgen receptor. This neuroprotective effect of testosterone varies according to the types of SOD1 gene mutation. These data suggest that testosterone may be of therapeutic value against ALS.

• The Korean Journal of Pain
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• v.28 no.1
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• pp.4-10
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• 2015

Etifoxine (etafenoxine, $Stresam^{(R)}$) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by $GABA_A{\alpha}2$ receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to ${\beta}2$ or ${\beta}3$ subunits of the $GABA_A$ receptor complex. It also modulates $GABA_A$ receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates $GABA_A$ receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.19-27
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• 1999

Apoptosis has been implicated in the pathophysiological mechanisms of various neurodegenerative diseases. In a variety of cell types, oxidative stress has been demonstrated to play an important role in the apoptotic cell death. However, the exact mechanism of oxidative stress-induced apoptosis in neuronal cells is not known. In this study, we induced oxidative stress in IMR-32 human neuroblastoma cells with tert- butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decrease in cell viability and increase in DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular $Ca^{2+}$ concentration, which was completely prevented either by EGTA, an extracellular $Ca^{2+}$ chelator or by flufenamic acid (FA), a non-selective cation channel (NSCC) blocker. These results indicate that the TBHP-induced intracellular $Ca^{2+}$ increase may be due to $Ca^{2+}$ influx through the activation of NSCCs. In addition, treatment with either an intracellular $Ca^{2+}$ chelator (BAPTA/AM) or FA significantly suppressed the TBHP-induced apoptosis. Moreover, TBHP increased the expression of p53 gene but decreased c-myc gene expression. Taken together, these results suggest that the oxidative stress-induced apoptosis in neuronal cells may be mediated through the activation of intracellular $Ca^{2+}$ signals and altered expression of p53 and c-myc.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.401-408
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• 2009

$K^+$-$Cl^-$-cotransport (KCC) has been reported to have various cellular functions, including proliferation and apoptosis of human cancer cells. However, the signal transduction pathways that control the activity of KCC are currently not well understood. In this study we investigated the possible role of phospholipase $A_2$ ($PLA_2$)-arachidonic acid (AA) signal in the regulatory mechanism of KCC activity. Exogenous application of AA significantly induced $K^+$ efflux in a dose-dependent manner, which was completely blocked by R-(+)-[2-n-butyl-6,7 -dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1Hinden-5-yl]oxy]acetic acid (DIOA), a specific KCC inhibitor. N-Ethylmaleimide (NEM), a KCC activatorinduced $K^+$ efflux was significantly suppressed by bromoenol lactone (BEL), an inhibitor of the calciumindependent $PLA_2$ ($iPLA_2$), whereas it was not significantly altered by arachidonyl trifluoromethylketone ($AACOCF_3$) and p-bromophenacyl bromide (BPB), inhibitors of the calcium-dependent cytosolic $PLA_2$ ($cPLA_2$) and the secretory $PLA_2$ ($sPLA_2$), respectively. NEM increased AA liberation in a doseand time-dependent manner, which was markedly prevented only by BEL. In addition, the NEM-induced ROS generation was significantly reduced by DPI and BEL, whereas $AACOCF_3$ and BPB did not have an influence. The NEM-induced KCC activation and ROS production was not significantly affected by treatment with indomethacin (Indo) and nordihydroguaiaretic acid (NDGA), selective inhibitors of cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Treatment with 5,8,11,14-eicosatetraynoic acid (ETYA), a non-metabolizable analogue of AA, markedly produced ROS and activated the KCC. Collectively, these results suggest that $iPLA_2$-AA signal may be essentially involved in the mechanism of ROS-mediated KCC activation in HepG2 cells.

• The Korean Journal of Physiology
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• v.10 no.1
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• pp.41-48
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• 1976

Tetrodotoxin (TTX) is the purified active principle responsible for tetrodon (Puffer-fish) poisoning which has long been known in the Orient. The pharmacological actions of TTX have been rather extensively investigated. Two of the most prominent effects of intravenousely administered TTX are severe hypotension and respiratory paralysis resulting from its depressant actions on tissues. This depressant actions of TTX in turn result from the selective inhibition of sodium-carrying mechanism which is essential to generation of the action potential. TTX differs from local anesthetics in that it does not affect potassium conductance. Although the mechanism of the hypotensive action of TTX remains a subject of controversy, most investigator agree that TTX-induced hypotension is caused by alteration in the blood vessels rather than the heart. Not only the study on the effects of TTX on cardiac function is meager but the results of reported works are often contradictory. The present study was undertaken to investigate the effect of TTX on the electrocardiogram of the rabbit and to compare them with well known electrocardiographical characteristics found in digitalis and quinidine intoxicated animals. The results obtained from the present study are summarized as follows. 1. No changes were found in P-R interval and QRS duration after i.v. administration of $1.0\;{\mu}g/kg\;to\;1.5\;{\mu}g/kg$ TTX to the animals. It is obvious that there were no conduction disturbance between atria and ventricles as well as in the ventricular tissue. 2. In $1.0\;{\mu}g/kg$ TTX group, S-T interval and T-P segment were not changed whereas marked changes were observed in $1.5\;{\mu}g/kg$ TTX group. 3. The first and second degree A-V blocks appeared in the $2.0\;{\mu}g/kg$ TTX group. 4. TTX differs from digitalis and quinidine in that it does not cause S-T interval depression and T-wave inversion. In contrast with digitalis, TTX caused Q-T interval prolongation.

• Journal of the Korean Chemical Society
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• v.9 no.4
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• pp.185-189
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• 1965

Korean acid clays and silica gel were put into action on benzene solution of dye, such as aniline yellow, o-nitro aniline and oil orange, and then the adsorptivity of dye in nonaqueous solution was measured, with the result that adsorptivity was greater with silica than acid clays and it had no relation to acidity. And when chemical compounds, such as amine, alcohol, halogen derivative, were added to each dye solution by 10%(in volume), the change of the adsorptivity of dye by solid acid(that is, the interfered adsorption rate) decreased in order of amine > alcohol > halogen derivative, and in homologue the smaller the molecular weight, the larger was the effect. So adsorption in nonaqueous solution was a selective adsorption of chemical compounds which contained negative groups such as amine and hydroxyl radicals, and it had no relation to surface tension and showed inverted phenomenon of Traube series. It is guessed that the inverted phenomenon (the interfered adsorption phenomenon) was due to the polar chemical adsorption between active $SiO_2$ which was an origin of solid acid and the adsorbed substances, considering that the order of inversion was nearly in accord with dipole moment of added solvents. The results of this study led to find adsorption mechanism and inverted phenomenon of Traube series in nonaqueous solution.

• Bulletin of the Korean Chemical Society
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• v.33 no.7
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• pp.2325-2332
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• 2012

A series $[C_3Omim]$[X] of imidazolium cation-based ILs, with ether functional group on the alkyl side-chain have been synthesized and structure of the materials were confirmed by various techniques like $^1H$, $^{13}C$ NMR spectroscopy, MS-ESI, FTIR spectroscopy and EA. More specifically, the influence of changing the anion with same cation is carried out. The absorption capacity of $CO_2$ for ILs were evaluated at 30 and $50^{\circ}C$ at ambient pressure (0-1.6 bar). Ether functionalized ILs shows significantly high absorption capacity for $CO_2$. In general, the $CO_2$ absorption capacity of ILs increased with a rise in pressure and decreased when temperature was raised. The obtained results showed that absorption capacity reached about 0.9 mol $CO_2$ per mol of IL at $30^{\circ}C$. The most probable mechanism of interaction of $CO_2$ with ILs were investigated using FTIR spectroscopy, $^{13}C$ NMR spectroscopy and result shows that the absorption of $CO_2$ in ether functionalized ILs is a chemical process. The $CO_2$ absorption results and detailed study indicates the predominance of 1:1 mechanism, where the $CO_2$ reacts with one IL to form a carbamic acid. The $CO_2$ absorption capacity of ILs for different anions follows the trend: $BF_4$ < DCA < $PF_6$ < TfO < $Tf_2N$. Moreover, the as-synthesized ILs is selective, thermally stable, long life operational and can be recycled at a temperature of $70^{\circ}C$ or under vacuum and can be used repeatedly.

• The Korean Journal of Pain
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• v.20 no.2
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• pp.92-99
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• 2007

Background: A correlation between a T-type voltage activated calcium channel (VACC) and pain mechanism has not yet been established. The purpose of this study is to find out the effect of ethosuximide and mibefradil, representative selective T-type VACC blockers on postoperative pain using an incisional pain model of rats. Methods: After performing a plantar incision, rats were stabilized on plastic mesh for 2 hours. Then, the rats were injected with ethosuximide or mibefradil, intraperitoneally and intrathecally. The level of withdrawal threshold to the von Frey filament near the incision site was determined and the dose response curves were obtained. Results: After an intraperitoneal ethosuximide or mibefradil injection, the dose-response curve showed a dose-dependent increase of the threshold in a withdrawal reaction. After an intrathecal injection of ethosuximide, the threshold of a withdrawal reaction to mechanical stimulation increased and the increase was dose-dependent. After an intrathecal injection of mibefradil, no change occurred in either the threshold of a withdrawal reaction to mechanical stimulation or a dose-response curve. Conclusions: The T-type VACC blockers in a rat model of postoperative pain showed the antihyperalgesic effect. This effect might be due to blockade of T-type VACC, which was distributed in the peripheral nociceptors or at the supraspinal level. Further studies of the effect of T-type VACC on a pain transmission mechanism at the spinal cord level would be needed.