• Bulletin of the Korean Chemical Society
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• 제15권4호
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• pp.270-272
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• 1994

• Bulletin of the Korean Chemical Society
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• 제19권3호
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• pp.279-281
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• 1998

• 생명과학회지
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• 제24권1호
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• pp.98-103
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• 2014

NQO1은 플라보 단백질 계통의 2 전자 환원 효소이며 NADH 또는 NADPH를 보조인자로 quinone 계통의 화합물을 hydroquinone으로 환원 한다. 암에서 NQO1은 그에 상응하는 정상 조직과 비교하였을 때 비교적 높은 발현을 나타낸다. NQO1의 다양한 기능 중 quinone 물질 대사는 두 가지 형태의 상반되는 기능을 가진다. 이것은 quinone으로부터 전환된 hydroquinone의 상태적 안정성과 불안정성에 기인하며, 불안정한 hydroquinone의 생성은 산화적 손상 야기 및 DNA 손상은 세포의 운명을 바꾸어 놓게 된다. 따라서 암에서 그 발현이 높은 NQO1을 표적으로 작용하는 생체환원 물질은 암 세포 사멸을 강하게 유도하게 되어 암 치료의 가능성을 보여주고 있다. 항암 표적 분자로서 NQO1 특징과 NQO1을 통해 작용하는 생체환원물질 ${\beta}$-lapachone의 항암 효과와 기전에 대하여 살펴보았다.

• 한국광과학회:학술대회논문집
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• 한국광과학회 2002년도 정기총회 및 제9회 광과학 학술심포지움 논문초록
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• pp.78-78
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• 2002

• Journal of Photoscience
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• 제4권2호
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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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• 제29권7호
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• pp.1418-1420
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• 2008

• Archives of Pharmacal Research
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• 제23권5호
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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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• 제15권2호
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• pp.103-104
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• 1994

• Toxicological Research
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• 제13권3호
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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.

• 약학회지
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• 제43권5호
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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.