• Journal of Photoscience
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• 제6권1호
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• pp.7-12
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• 1999

Irradiation of 1 , 4-diphenylbut-1-en-3-yne 1 and some p-quinones in dichloromethane with 300nm UV light yield tow types of adducts, i.e., p-quinomethanes and cyclobutanes, in which the former were produced via the rearrangement of the intially formed spiro-oxetene intermediates. On the other hadn 1 added to o-quinones to give three types of adducts, i.e., 1, 3-dienes, 1, 4-dioxenes, or spiro-oxetanes, in which the former were found to be applied to synthesize phenanthrene derivatives. A methoxy derivative of enyne 39 was synthesized to investigate the type of thephotoaddition to o-quinones, in which 1, 4-dioxenes were obatained.

• Journal of Photoscience
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• 제3권2호
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• pp.61-64
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• 1996

Photoaddition reactions of p-quinones to 1, 4-diphenylbubl-en-3-yne (BEY) have been investigated. Irradiation (300 nm) of BEY and 1, 4-benzoquinones in dichloromethane afforded quinone methides. I rradiation of 1, 4-naphthoquinone and BEY leaded to the formation of unstable spiro oxetene intermediate, followed by the rearrangement to give quinone methide, and finally the oxidative photocyclization. In contrast, irradiation 2, 3-dichloro-1, 4-naphthoquinone (or anthraquinone) and BEY yielded another type of quinone methides in one pot.

• Bulletin of the Korean Chemical Society
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• 제10권1호
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• pp.66-69
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• 1989

Irradiation of solutions of p-quinones and conjugated diyne, 1,4-diphenylbutadiyne, with 350 nm UV light gave the photoproducts such as quinomethane in good yields (70-85%).

• Bulletin of the Korean Chemical Society
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• 제19권12호
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• pp.1295-1297
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• 1998

• BMB Reports
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• 제48권11호
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• pp.609-617
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• 2015

NAD(P)H:quinone oxidoreductase (NQO1), an obligatory two-electron reductase, is a ubiquitous cytosolic enzyme that catalyzes the reduction of quinone substrates. The NQO1- mediated two-electron reduction of quinones can be either chemoprotection/detoxification or a chemotherapeutic response, depending on the target quinones. When toxic quinones are reduced by NQO1, they are conjugated with glutathione or glucuronic acid and excreted from the cells. Based on this protective effect of NQO1, the use of dietary compounds to induce the expression of NQO1 has emerged as a promising strategy for cancer prevention. On the other hand, NQO1-mediated two-electron reduction converts certain quinone compounds (such as mitomycin C, E09, RH1 and β-lapachone) to cytotoxic agents, leading to cell death. It has been known that NQO1 is expressed at high levels in numerous human cancers, including breast, colon, cervix, lung, and pancreas, as compared with normal tissues. This implies that tumors can be preferentially damaged relative to normal tissue by cytotoxic quinone drugs. Importantly, NQO1 has been shown to stabilize many proteins, including p53 and p33ING1b, by inhibiting their proteasomal degradation. This review will summarize the biological roles of NQO1 in cancer, with emphasis on recent findings and the potential of NQO1 as a therapeutic target for the cancer therapy.

• 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.

• 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.

• 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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• 제29권7호
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• pp.1418-1420
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• 2008

• 약학회지
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• 제41권6호
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• pp.829-836
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• 1997

Studies on the effect of quinones on cardiac function has been conducted with normal hearts. But not with injured hearts, I.e. ischemia/reperfusion-injured heart. Quinone compounds are known to produce oxygen free radicals during metabolism, and for this reason, quinones are implicated in the aggravation of ischemia/reperfusion injury or cardioprotection, as in the case of ischemic preconditioning depending on the experimental conditions. The present study was carried out to examine the effect of 2-chloro-3-(4-cyanophenylamino)-1.4-naphthoquinone (NQ-Y15) on cardiac function of ischemic/reperfused and normal rat hearts. In isolated perfused hearts, various functional parameters such as left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (EDP) and maximum positive and negative dP/dt ($[\pm}dP/dt_{max}$), time to contracture, heart rate (HR) and coronary flow rate (CFR) were measured before and 30 min after dosing and following 25 min ischemia/30min reperfusion. NQ-Y15 increased LVDP, +dP/$d_{max}$and -dP/$dt_{min}$ by 18%. 30%, and 40%, respectively. There were no significant changes in other haemodynamic parameters. After ischemia/reperfusion injury, pretreatment with NQ-Y15 induced a significant decrease in LVDP and $[\pm}dP/dt_{max}$, but an increase in EDP. LDH-release was not significantly increased. These results suggested that NQ-Y15 may augment the ventricular contractility but it makes hearts more vulnerable to ischemia/reperfusion injury.