• The korean journal of orthodontics
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• v.23 no.2 s.41
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• pp.147-163
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• 1993

The purpose of this stuy was to evaluated the cytotoxicity of brackets which were recycled thermally or chemically. New brackets and used brackets which had been in mouth for at least 2years were used as samples and human gingival cell culture and agar overlay technique was used to evaluate the cytotoxicity. From the experiment the following results were obtained : 1. New brackets in the as received state showed mild cytotoxicity. 2. Thermally recycled brackets except the used bracket not electropolished showed moderate cytotoxicity and among them new brackets showed greater cytotoxicity than used ones. 3. Used brackets which were thermally recycled without electropolishing showed mild cytotoxicity. 4. Among thermally recycled brackets, electropolished brackets showed greater cytotoxicity than not electro-polished ones. 5. Chemically recycled brackets showed moderate cytotoxicity, and among them, new brackets appeared to be more cytotoxic than used ones.

• Biomedical Science Letters
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• v.23 no.4
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• pp.339-347
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• 2017

This study was performed to evaluate the cytotoxicity induced by ischemia-like condition (ILC) in cultured neuroglial cells (C6 glioma cells). The protective effect of kaempferol (KAE), flavonoid against the cytotoxicity induced by ILC induction was assessed. In addition, antioxidative effects of KAE were done by colorimetric assays. Cell viability and the antioxidative effects such as DPPH-radical scavenging activity, superoxide dismutase (SOD)-like activity and inhibitory activity of lipid peroxidation (LP) were analyzed. ILC induction decreased cell viability in a dose-dependent manner, and the $XTT_{90}$ value (low cytotoxicity value) and $XTT_{50}$ value (high cytotoxicity value) were determined during ILC induction for 15 and 40 minutes, respectively. The butylated hydroxytoluene (BHT) antioxidant significantly increased cell viability damaged by the ILC-induced cytotoxicity. In the protective effect of KAE on ILC-induced cytotoxicity, KAE protected the ILC-induced cytotoxicity by the significant increase of cell viability, and also it showed DPPH-radical scavenging ability, SOD-like ability and inhibitory ability of LP. From these results, it is suggested that ILC induction showed cytotoxicity in these cultures and the oxidative stress is involved in the ILC-induced cytotoxicity. While, KAE prevented ILC-induced cytotoxicity by antioxidative effects. In conclusion, natural products like KAE may be a putative therapeutic agent for the treatment of disease associated with oxidative stress such as ischemia.

• Toxicological Research
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• v.16 no.4
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• pp.311-315
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• 2000

Previous studies showed that benzoquinone derivatives inhibited platelet aggregation. but there is no information available on their cytotoxicity to platelets. 1n the present study. washed platelets isolated from rats were treated with 1.4-benzoquinone. a representative benzoquinone derivative. to examine its antiaggregating effect and cytotoxicity. 1.4-Benzoquinone significantly inhibited thrombin-induced platelet aggregation. Consistent with this finding. 1.4-benzoquinone suppressed cytosolic calcium increase induced by thrombin. To examine the cytotoxicity by 1 A-benzoquinone in platelets. turbidometry and lactate dehydrogenase release were measured. Treatment with 1.4-benzoquinone resulted in slight cytotoxicity (30% release at 60 min) to platelets. However. the cytotoxicity was not correlated with increase of cytosolic calcium levels in platelets. All these data suggested that 1.4-benzoquinone inhibited thrombin-induced platelet aggregation mediated by inhibition elf calcium level increase and that 1.4-benzoquinone reveals cytotoxicity to some extent without alteration of calcium level in platelets.

• Natural Product Sciences
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• v.19 no.4
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• pp.329-336
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• 2013

The purpose of this study is to evaluate cytoprotective effect of Korean medicinal plants on alcohol-induced cytotoxicity in liver cells. Out of the 120 plant extracts tested in this study, 53 plant extracts enhanced alcohol-induced cytotoxicity in liver cells by 50~80%, while other 11 plant extracts including Crataegus pinnatifida reduced cytotoxicity by 1~68%. The results of DPPH free radical test and LDL lipid peroxidation test on the plant extracts that sharply reduced cytotoxicity in liver cells shows that Crataegus pinnatifida and Cinnamomum cassia had antioxidative effect. This study reports that the plant extracts that enhance or reduce ethanol-induced cytotoxicity in liver cells can be research objects as cytotoxic plants or cytotoxicity-protective plants.

• Parasites, Hosts and Diseases
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• v.38 no.2
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• pp.99-102
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• 2000

In order to observe the cytotoxicity of Acanthamoeba spp., which were isolated from contact lens containers as ethiological agents for the probable amoebic keratitis in Korea, the crystal violet staining method and LDH release assay were carried out. In the crystal violet staining method, among eight contact lens container isolates, isolate 3 (Acanthauloeba KA/LS5) showed 83.6% and 81.8% of cytotoxicity, and isolate 7 (Acanthamoeba KA/LS37) showed 28.2% and 25.1% of cytotoxicity, in 1 mg/ml and 0.5 mg/ml Iysate treatments, respectively. Acanthamoeba cutbertsoni and A. healyi showed 84.0% and 82.8% of cytotoxicity. Similar results were observed in A. costellunii and A. hafchefti which showed 83.6% and 75.5% or cytotoxicity. Acanthamoeba roureba and A. polyphaga showed 9.0% and 1.7% of cytotoxicity. In the LDH release assay, isolate 3 (20.4%) showed higher cytotoxicity than other isolates in 1 mg/ml Iysate treatment. The results provide that at least isolate 3 has the cytotoxic effect against CHO cells and seems to be the pathogenic strain.

• BMB Reports
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• v.29 no.4
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• pp.314-320
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• 1996

The effects of non-cytotoxic concentrations of tamoxifen, verapamil, and trifluoperazine on doxorubicin cytotoxicity in five human breast cancer cell lines were studied. A non-cytotoxic concentration of tamoxifen resulted in enhanced doxorubicin cytotoxicity in HTB-123, HTB-26, and MCF-7. In these three cell lines, a combination of tamoxifen with verapamil resulted in even more increased doxorubicin cytotoxicity. Addition of verapamil or trifluoperazine alone did not influence the doxorubicin cytotoxicity significantly. Only in HTB-19 did coincubation with verapamil increase the doxorubicin cytotoxicity. In HTB-123, combination of tamoxifen with trifluoperazine increased the doxorubicin cytotoxicity significantly. In the cell lines where co-incubation with tamoxifen increased doxorubicin sensitivity, high estrogen receptor expression was detected. However, HTB-20, where tamoxifen did not enhance doxorubicin action, was also estrogen receptor positive. None of the cell lines had multidrug resistance related drug efflux and drug retention was not increased by the treatment with tamoxifen and verapamil. Cell cycle traverses were not altered by incubation with tamoxifen, verapamil or combinations thereof. These observatlons suggest mechanism of non-cytotoxic concentrations of tamoxifen and verapamil on doxorubicin cytotoxicity may involve one or more other cellular processes besides those of interference of estrogen binding to its receptor, cell cycle perturbation, or drug efflux blocking.

• Restorative Dentistry and Endodontics
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• v.16 no.2
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• pp.62-84
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• 1991

The purpose of this study was to evaluate the cytotoxicity of four root canal sealers(Tubliseal, AH26, Apatite Root Canal Sealer I, Apatite Root Canal Sealer II) in Vitro. The root canal sealers were mixed and filled in molds which were $14{\times}1.25mm$ in diameter, in height to use for cell counting and agar overlary method, and $7{\times}1.25mm$ for millipore filter method and set for 7 days to use for experiment. Silicone and copper plate were used for negative and positive control respectively. Using the culture of L929 fibroblast, total cell number and vital cell number were counted and the ratio of vital cell number to total cell number was calculated on 2 nd, 4 th, 6 th experimental day, and the change of cell membrane permeability was tested by agar overlay method, and the succinate dehydrogenase activity was tested by millipore filter method. The obtained results were as follows. 1. In ail experimental groups, the mitotic activity of fibroblast was reduced when compared with that of negative control group, so ail experimental groups showed cytotoxicity. Apatite Root Canal Sealer I group exhibited mild cytotoxicity, and Tubliseal, AH26, Apatite Root Cenal Sealer II groups exhibited severe cytotoxicity. 2. In the test of the change of cell membrane permeability by agar overlay method, all experimental groups showed cytotoxicity. AH26 group exhibited mild cytotoxicity, and Apatite Root Canal Sealer I group exhibited moderate cytotoxicity, and Tubliseal and Apatite Root Canal Sealer II group exhibited severe cytotoxicity. 3. In the test of SDH activity by millipore filter method, there was no cytotoxicity in Apatite Root Canal Sealer I and Apatite Root Canal Sealer II group, but Tubliseal and AH26 group showed mild cytotoxicity.

• Archives of Pharmacal Research
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• v.19 no.1
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• pp.12-17
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• 1996

Our previous studies demonstrate that menadione (MEN) is cytotoxic to platelets of rats by depleting glutathione (GSH). In order to clarify whether GSH has a role in protecting against menadione-induced cytotoxicity, the effect of GSH depletors as well as GSH precusors on menadione-induced cytotoxicity was investigated. Cysteine and dithiothreitol (DTT) prevent MEN-induced cytotoxicity in a dose-dependent manner, as determined by LDH leakage and change in turbidity. When platelets were treated with 1-chloro-2,4-dinitrobenzene (CDNB) and diethylmaleate (DEM), both of which deplete intracellular GSH, MEN-induced cytotoxicity was potentiated in the CDNB-treated paltelets, but not in the DEM-treated platelets. These data suggest that the GSH in platelets plays an important role in protecting against cytotoxicity induced by menadione.

• 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.

• Toxicological Research
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• v.11 no.2
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• pp.303-308
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• 1995

Nitric oxide, a physiological transmitter, is reported to mediate cellular injury in various tissues. Its reactivity to free radical is believed to be one of the reasons for its involvement in cytotoxicity. Menadione, a representative quinone, is cytotoxic to several cell systems including isolated hepatocyte, endothelial cell and red blood cells. Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals. Our previous studies demonstrated that menadione induced cell lysis and increase of oxygen consumption in platelets. It has been reported that platelets have nitric oxide producing enzyme, nitric oxide synthase. Thus, we have investigated to manifest the role of nitric oxide.in menadione-induced cytotoxicity in rat platelets. Menadione induced cytotoxicity in platelets was unaffected by $N^G$-nitro-arginine methyl ester (L-NAME), selective and competitive inhibitor of nitric oxide synthase. We also invesitgated the role of extracellular nitric oxide in menadione-induced cytotoxicity of platelets by addition with sodium nitroprusside (SNP). SNP did not affect platelet cytotoxicity by menadione. These results suggested that nitric oxide which was generated endogeneously or exogeneously might have a negligible role in menadione-induced cytotoxicity in rat platelets.