• Bulletin of the Korean Chemical Society
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• v.15 no.4
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• pp.270-272
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• 1994

• Bulletin of the Korean Chemical Society
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• v.19 no.3
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• pp.279-281
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• 1998

• Journal of Life Science
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• v.24 no.1
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• pp.98-103
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• 2014

NAD(P)H quinone oxidoreductase 1 (NQO1) is a flavoprotein that catalyzes the two electron reduction of diverse substrates, including quinones. It uses NADH or NADPH as a cofactor for enzymatic machinery. In the metabolism of quinones, NQO1 has two conflicting functions because of the different stability of converted hydroquinones. The stable form of hydroquinone is excreted from cells by conjugation with glutathione or glucuronic acid. The unstable form of hydroquinone induces cell death by induction of oxidative stress and DNA damage. Certain quinones known as bio-reductive agents have a cytotoxic function following reduction by NQO1. Bio-reductive agents, such as ${\beta}$-lapachone or mitomycin C, induce the depletion of NAD(P)H and the generation of oxidative stress in an NQO1-dependent manner. NQO1 is highly expressed in several cancer tissues. Therefore, NQO1 is a good therapeutic target for cancer treatment with bio-reductive agents.

• Proceedings of the Korean Society of Potoscience Conference
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• 2002.06a
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• pp.78-78
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• 2002

• Journal of Photoscience
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• v.4 no.2
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• pp.49-52
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• 1997

Irradiation (300 nm) of 1, 2-benzoquinones 1 and diphenylacetylene 2 in dichloromethane yielded two isomeric quinone methides, 6 and 7. The same types of quinone methides, 9 and 10 (or 12 and 13) were obtained from the photocycloadditions of 9, 10-phenanthrenequinone 8 (or acenaphthenequinone 11) to diphenylacetylene 2. One-way photoisomerizations were observed between each isomeric adducts, (6, 7), (9, 10) and (12, 13).

• Bulletin of the Korean Chemical Society
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• v.29 no.7
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• pp.1418-1420
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• 2008

• Archives of Pharmacal Research
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• v.23 no.5
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• pp.446-449
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• 2000

Imidazonaphthothiazole derivatives 3∼6 were prepared by treatment of 2-aminonaphtho[2,3-d]-thiazole-4,9-dione(1) with phenacyl bromide, chloroacetic acid, diethyl oxalate and 2,3-dichloroquinoxaline respectively. The reaction of 1 with ethyl acrylate, ethyl acetoacetate and diethyl malonate gave the corresponding naphthothiazolopyrimidine derivatives 8∼11.

• Bulletin of the Korean Chemical Society
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• v.15 no.2
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• pp.103-104
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• 1994

• Toxicological Research
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• v.13 no.3
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• pp.223-228
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• 1997

Quinones have been reported to undergo nonenzymatic reaction with thiols to generate reactive oxygens. It is therefore possible that the nonenzymatic reaction of quinones with thiols in plasma could lead to potentJared cellular toxicity or disease. When 1 mM menadione was added in plasma under pH 11.2, 7.4 and 5.0, the increase in oxygen consumption rate was the order of pH 11.2 > pH 7.4 > pH 5.0. In addition, oxygen consumption rates under plasma anticoagulated with trisodium citrate solution (pH 7.85) was significantly higher than those with acid-citrate-dextrose solution (pH 6.87). SOD and catalase reduced the rate of oxygen consumption induced by menadione in plasma. Taken together, these results suggest that the menadione-induced increased oxygen consumption was due to nonenzymatic reaction of menadione with thiols in the plasma. The presence of plasma has an additive effect on the increased oxygen consumption rates induced by the menadione treatments on our model tissue, platelets, as compared between washed platelet (WP) and platelet rich plasma (PRP). Cytotoxicity, as determined by LDH release, are well correlated with the oxygen consumption rates observed in each system and strongly suggest that menadione-induced cytotoxicity can be increased with the presence of blood plasma.

• YAKHAK HOEJI
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• v.43 no.5
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• pp.652-658
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• 1999

To reveal the inhibitory mechanism of NO-dependent vasorelaxation by quinone derivatives (OQ1 and OQ21), we have compared the generation of free radicals by oxidative stress and the formation of cellular adducts by arylation. First, we measured oxygen consumption by quinone derivatives as a marker of oxidative stress in order to investigate whether these quinone compounds could generate reactive oxygen species. Both OQ1 and OQ21 generated free radicals and OQ21 was more potent. These results suggested that free radicals be involved in the inhibition of vasorelaxation by quinones. Next, we measured the binding capacity of quinone derivatives with intracellular GSH and protein thiols (-SH) in order to investigate whether these quinones have arylation capacity. Compared to positive control groups (menadione), both OQ1 and OQ21 depleted intracellular GSH and protein thiols very slightly. These compounds have low toxicities in mammalian tissues. From these results, we concluded that the inhibition of vasorelaxation by quinone derivatives (OQ1, OQ21) may be cuased by generation of free radicals.