• The Korean Journal of Pesticide Science
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• v.5 no.1
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• pp.36-45
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• 2001

This study was conducted to search new target enzymes of novel herbicide candidate. Total of 107 biochemical inhibitors reported to inhibit over than 100 different plant enzymes were purchased from commercial chemical companies. 15 inhibitors and 34 enzymes were selected by germination assay, seedling assay, wheat leaf disc assay, and whole plant assay. Among them, seven compounds of purine, phehyl-hydrazine, o-phenanthroline, oleylamine, dicyclohexylcarbodiimide, 7,8-benzoquinoline, and aminooxyacetic acid showed high herbicidal activity in the whole plant assay under greenhouse while 7,8-benzoquinone, 8-hydroxyquinoline, 2,2'-dipyridyl, and o-phenanthroline inhibited seed germination of barnyardgrass, rice, and tomato at concentrations of 1.25 to $5{\mu}M$. The compounds of 7,8-benzoquinoline, chlorpromazine, cyanuric fluoride, 4-methylpyrazole, oleylamine, tranylcypromine, and trifluoperazine inhibited the growth of cyanobacteria at 30 to $100{\mu}M$. The compounds of dicyclohexylcarbodiimide and chlorpromazine exhibited whitening effect on tile wheat leaf disc at $100{\mu}M$. These results suggest that the plant-specific enzyme inhibitors which have biological activities may supply the target enzyme for developing new herbicide candidate.

• Journal of Food Hygiene and Safety
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• v.13 no.3
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• pp.232-237
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• 1998

The purpose of this study is to examine the phototoxicity of four phenothiazine derivatives such as chlorpromazine, perphenazine, trifluoroperazine and promethazine, and to investigate the effects of ascorbic acid on their phototoxicity by UVB irradiation. Effects of the test compounds on RBCs were monitored with a spectrophotometer by the method of Kahn et al. The extent of photohemolysis by tested phenothiazine derivatives were increased with their concentration and toxic photoproducts were formed by chlorpromazine and promethazine with preirradiated UVB. Photohemolysis postirradiated chlorpromazine and perphenazine and preirradiated promethazine were decreased with the use of ascorbic acid significantly.

• Clinical and Experimental Reproductive Medicine
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• v.21 no.1
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• pp.111-119
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• 1994

"Spontaneous" hardening of the zona pellucida of mouse oocytes during in vitro culture is most likely due to cortical granules exocytosis. Thus the purpose of the present study was to determine whether the exocytosis factor is involved in spontaneous zona pellucida hardening during in vitro culture of the mouse. The results obtained form these experiments were summarized as follows; 1. When a protein synthesis inhibitor(100${\mu}g$/ml puromycin) was added to the culture medium, it did not prevent spontaneous ZPH of mouse oocyte during in vitro culture. 2. Calmodulin antagonists (trifluoperazine and chlorpromazine) and calcium channel blocker (verapamil) had no inhibitory effect in spontaneous ZPH. 3. A microtubule assembly inhibitor, colcemid had some inhibitory effect on spontaneous ZPH. 4. Treatment with a microfillament formation blocker(cytochalasin-B) at 1${\mu}g$/ml concentration, resulted in the excellent inhibitory effect on spontaneous ZPH. However cytochalasin-B did not inhibit ethanol-induced ZPH.

• BMB Reports
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• v.28 no.1
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• pp.79-82
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• 1995

Exposure of spleen lymphocytes to 2-chloroethylethyl sulfide (CEES) leads to a reduction of the intracellular ATP level, followed by a decrease in cell viability. Addition of nicotinamide, an inhibitor of poly(ADP-ribose) polymerase (PADPRP), restores both ATP level and viability, indicating that an activation of PADPRP is responsible for the cytotoxicity of CEES. The involvement of a $Ca^{2+}$-mediated process in cytotoxicity is suggested. Verapamil, EGTA, trifluoperazine, and butacaine exhibit a partial protection (20 to 58%) against the cytotoxicity of CEES. Investigation of the causative role of proteolytic degradation in cell death indicate that pepstatin and leupeptin exert a substantial protective effect (60 to 70%), suggesting the involvement of lysosomal destabilization in CEES-induced cytotoxicity. Also, lysosomotropic agents markedly decrease the cytotoxicity. Lysosomal labilization may be a mechanism for the cytotoxicity of CEES.

• The Korean Journal of Physiology
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• v.20 no.2
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• pp.236-248
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• 1986

Alterations of renin-angiotensin system have been suggested as one of the mechanisms increasing arterial blood pressure in experimental and clinical hypertension. But the exact nature of high blood pressure in the early and late phase of renal hypertension is still controversial. To clarify the nature of renin release in both unclipped and clipped kidney of two kidney one clip Goldblatt lypertensive rat, experiments have been done in kidney slices, which were obtained from the rats of 3 and 7 days of operation. Basal rate of renin release was suppressed in unclipped kidney slices compared to clipped kidney Norepinephrine increased renin release from unclipped kidney slices, but not from clipped kidney slices. Suppressions by angiotensin Il and arginine vasopressin of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. Increases by verapamil and trifluoperazine of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. These results suggest that the negative feedback control mechanism of the renin-angiotensin system by angiotensin Il and arginine vasopressin is attenuated in the clipped kidney of two kidney one clip Goldblatt hypertensive rat, and that one of the altered mechanisms may be caused by certain regulatory changes of intracellular calcium and/or calcium-calmodulin complex in the juxtaglomerular cells.

• YAKHAK HOEJI
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• v.33 no.4
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• pp.211-218
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• 1989

Twenty-six injectable drug products, many of which are administered by i.v. infusion, were studied for loss from aqueous solutions stored in polyvinyl chloride (PVC) infusion bags for various periods of time. The PVC infusion bags were stored in the dark room at room temperature for up to one month. Drugs stored in glass bottle served as controls. The solutions were assayed Spectrophotometrically at regular intervals. The effect of drug concentration and pH on the loss of drug from solution were studied. Octanol-water partition coefficients were used as a guage of lipid solubility of drugs. The elution of di(2-ethylhexyl)phthalate(DEHT) from PVC infusion bags was studied. For most of the drug studied, minimal loss from the aqueous solutions were observed over periods of storage time. Six of the drug products - Thiopental sodium, Hydralazine HCl, Thioridazine HCl, Trifluoperazine 2HCl, Metronidazole, Chlorpromazine HCl - were found to be lost a substantial extent. DEHP was found to be migrating from PVC infusion bags.

• Journal of Plant Biotechnology
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• v.34 no.3
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• pp.213-221
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• 2007

The treatment of radish cotyledons with a nitric oxide (NO)-releasing substance, sodium nitroprusside (SNP) resulted in an increased adventitious root development in a dose-dependent manner. However, this NO-mediated enhancement effect was reversed when either 0.5 mM EGTA (an extracellular $Ca^{2+}$ chelator) or 0.1 mM $LaCl_3$ (a calcium channel blocker) was applied with $50\;{\mu}M$ SNP. Our results also showed that guaiacol peroxidase (GPX) and syringaldazine peroxidase (SPX) activities, which are known to play a key role in rooting, were more largely increased during adventitious root induction in the cotyledons treated with SNP. However, the treatment of cotyledons with SNP plus $LaCl_3$ inhibited the SNP-induced increases in the activities of both GPX and SPX. Trifluoperazine (TFP), an antagonist of calmodulin (a specific calcium-binding protein), also delayed adventitious root formation and significantly reduced the root length and number of the SNP-treated cotyledons as well as the deactivation of GPX and SPX enzymes. In conclusion, our results suggest that calcium is involved in the NO response leading to induction of adventitious root through a regulation of GPX and SPX.

• Journal of Microbiology and Biotechnology
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• v.14 no.3
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• pp.456-465
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• 2004

$K^+$ efflux through a certain type of $K^+$ channels causes the change of membrane potential and leads to cAMP synthesis in the transmembrane cell signaling for the initiation of sperm motility in the salmonid fishes. The addition of $Ca^{2+}$ conferred motility to the trout sperm that were immobilized by external $K^+$ and other alkaline metals, $Rb^+$ and $Cs^{2+}$, suggesting the participation of external $Ca^{2+}$ in the initiation of sperm motility. L-type $Ca^{2+}$ channel blockers such as nifedipine, nimodipine, and FS-2 inhibited the motility, but N-type $Ca^{2+}$ channel blocker, w-conotoxin MvIIA, did not. On the other hand, the membrane hyperpolarization and cAMP synthesis were suppressed by $Ca^{2+}$ channel blockers, nifedipine, and trifluoroperazine. Furthermore, these suppressions were relieved by the addition of $K^+$ ionophore, valinomycin. Inhibitors of calmodulin, such as W-7, trifluoperazine, and calrnidazol-C1, inhibited the sperm motility, membrane hyperpolarization, and cAMP synthesis. The results suggest that $Ca^{2+}$ influx through $Ca^{2+}$ channels that are sensitive to specific $Ca^{2+}$ channel blockers and calmodulin participate in the changes of membrane potential, leading to synthesis of cAMP in the cell signaling for the initiation of trout sperm motility.

• YAKHAK HOEJI
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• v.33 no.1
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• pp.1-9
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• 1989

We have recently reported that $Mg^{++}-deficiency$ showed endothelium dependent relaxation in isolated canine coronary arteries precontracted with $PGF_{2{\alpha}}$. To differentiate the release of EDRF or $PGI_2$ from the endothelium cells as the cause of vasorelaxation by $Mg^{++}-deficiency$, effects of several inhibitors of arachidonic acid metabolism on the relaxation by $Mg^{++}-deficiency$ were evaluated and also compared with that of acetylcholine. Ibuprofen and tranylcypromine ($10{\mu}M$), an inhibitor of cyclo-oxygenase and $PGI_2$ synthetase, respectively, did not effect on $Mg^{++}-free$ induced vasorelaxation. Pretreatment of quinacrine ($10{\mu}M$), an inhibitor of phospholipase $A_2$ and also $Ca^{++}$ uptake, blocked vasorelaxation by $Mg^{++}-free$. But trifluoperazine ($10{\mu}M$), which is about as potent as quinacrine in the inhibition of $Ca^{++}$ uptake, did not effect on $Mg^{++}-deficiency$ induced vasorelaxation. NDGA ($10{\mu}M$), an inhibitor of lipoxygenase, completely restored $Mg^{++}-free$ induced vasorelaxation, even though pretreatment of that was not blocked which might be due to the characteristics of vasorelaxation of NDGA itself. Pretreatment of methylene blue ($10{\mu}M$), which is known as a inhibitor of EDRF through the blocking effect of guanylate cyclase, completely blocked vasorelaxation by $Mg^{++}-free$ as well as acetylcholine ($0.1{\mu}M$). Acetylcholine-induced dose response curve was also antagonized by pretreatment of quinacrine ($10{\mu}M$), but not by ibuprofen, tranylcypromine and NDGA. These results appear to suggest that $Mg^{++}-free$ induced vasorelaxation was mediated by the release of EDRF through the activation of phospholipase $A_2$ and noncyclo-oxygenase on arachidonate metabolism.

• Toxicological Research
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• v.20 no.3
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• pp.241-250
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• 2004

We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration. Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic agents which cause increase of intracellular calcium level, BPA decreased $[Ca^{2+}]_i$ dose-dependently in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at greater concentrations than 100 $\mu\textrm{M}$ reduced cell viability significantly in both types of cells. BPA also suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist, 30 $\mu\textrm{M}$)-induced increase of $[Ca^{2+}]_i$. BPA further lowered caffeine (RYR activator, 100 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$, but did not alter dantrolene (RYR inhibitor, 100 $\mu\textrm{M}$), heparin (IP3 inhibitor, 200 units/ml) and xestospongin C (IP3 inhibitor, 5 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$. Cell viability was not directly related to intracellular calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal factor of BPA-induced neuronal cell death.