• 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.

• Bulletin of the Korean Chemical Society
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• 제24권2호
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• pp.153-154
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• 2003

• Applied Biological Chemistry
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• 제11권
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• pp.29-33
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• 1969

1. $NADPH_2$산화효소존재하(酸化酵素存在下)에 있어서 Quinone에 의(依)한 $NADPH_2$의 산화(酸化)를 시험관내(試驗管內)에서 조사(調査)하였다. 그 결과(結果)를 $3{\times}10^{-5}M$.의 각종(各種) Quinone 류(類)로 $^{14}CO_2$고정(固定) 10분전급고정시험중(分前及固定試驗中) 처리(處理)한 Chlorella의 $^{11}CO_2$고정율(固定率)과 비교(比較)하였다. 2. 각종(各種) Quinone 류(類)의 $NADPH_2$ 산화속도(酸化速度)와 $^{14}CO_2$ 고정율(固定率)사이에는 밀접(密接)한 관계(關係)가 있음이 밝혀졌다. $NADPH_2$ 산화(酸化)와 $^{14}CO_2$ 고정(固定)에 대(對)한 Quinone의 영향(影響)은 그 세기가 다음 순서(順序)와 같다. Dichlone>06-K>NQ>BQ 3. Chlorella에 대(對)한 Quinone의 독성(毒性)은 NADPH를 식물체(植物體)에서 없앰으로서 $^{14}CO_2$ 고정(固定)을 방해(妨害)하여 세포(細胞)를 결과적(結果的)으로 죽이는 것이라고 생각이된다. 4. Chlorella의 아미노산(酸) 생합성(生合成)에 대(對)한 Quinone류(類)의 영향(影響)은 전반적(全般的)으로 이를 억제(抑制)하는 것이라 하겠다. 이것은 특(特)히 Dichlone에 있어서 현저(顯著)하다. 이 현상(現象)은 식물(植物)에 $NADPH_2$가 없어지고 $^{14}CO_2$고정(固定)이 조해(阻害)되기 때문일 것이다. 자당(蔗糖)의 생합성(生合成)은 영향(影響)을 받지않거나 오히려 자극(刺戟)을 받는데 그 이유(理由)는 불분명(不分明)하다.

• 대한의생명과학회지
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• 제24권3호
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• pp.143-149
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• 2018

Excessive exposure to estrogens is the most important risk factor for the development of hormone-sensitive cancers, especially breast cancer. Estrogen stimulates the expression of genes and proteins involved in cell proliferation by binding to estrogen receptor (ER). Another possible mechanism of ER-independent carcinogenicity of estrogens is based on the hydroxylation of estradiol resulting in the formation of catechol estrogens. Catechol estrogen 4-hydroxyestradiol ($4-OHE_2$) is further oxidized to catechol estrogen-3,4-quinones, the major carcinogenic metabolites of estrogens. Evidence increasingly supports the critical role of $4-OHE_2$ in hormonal carcinogenesis via DNA adduct formation or production of reactive oxygen species, which finally contribute to the transformation of normal mammary epithelial cells and the enhanced growth of breast cancer cells. It is also reported that the level of $4-OHE_2$ or its quinones is highly up-regulated in urine or tissues of breast cancer patients. Thus, we highlight the oncogenic roles of $4-OHE_2$ in catechol estrogen-induced breast carcinogenesis.

• Toxicological Research
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• 제12권2호
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• pp.289-293
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• 1996

Our previous studies demonstrated that quinone (menadione) is cytotoxic to rat platelets. In an attempt to assess the relative contributions of redox cycling and/or arylation in quinone-induced cytotoxicity, we have studied three quinones with different mechanisms: 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ; pure redox cycler), menadione (both redox cycler and arylator), and 1, 4-benzoquinone (pure arylator). The order of redox cycling capacity in platelet rich plasma (PRP) isolated from rats was menadione>DMNQ>1, 4-benzoquonone, which was consistent with the previous studies using isolated hepatocytes. 1, 4-Benzoquinone was more toxic to rat platelets than menadione, while DMNQ did not cause cell death at all. Lactate dehydrogenase inhibition studies revealed that 1, 4-benzoquinone inhibited significantly in a time-dependent manner, while menadione and DMNQ did not at all. These results suggested that arylation by quinone compounds might play a critical role in quinone-induced cytotoxicity in rat platelets.

• 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.

• Asian Journal of Atmospheric Environment
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• 제1권1호
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• pp.28-35
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• 2007

Accumulated epidemiological and animal studies have suggested that prolonged exposure to ambient particulate matter (PM) is associated with an increased risk of cardiovascular disease and pulmonary dysfunction. While diesel exhaust particles (DEP) contain large variety of compounds, polycyclic aromatic hydrocarbons (PAHs) are a dominant component contaminated in DEP. This article reviews effects of two PAH quinones, 9,10-phenanthraquinone (9,10-PQ) and l,2-naphthoquinone (l,2-NQ), on vascular and respiratory systems.

• 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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• 제32권5호
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• pp.1679-1684
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• 2011

Interfacial reactions kinetics often differ from kinetics of bulk reactions. Here, we describe how the density change of an immobilized reactant influences the kinetics of interfacial reactions. Self-assembled monolayers (SAMs) of alkanethiolates on gold were used as a model interface and the Diels-Alder reaction between immobilized quinones and soluble cyclopentadiene was used as a model reaction. The kinetic behavior was studied using varying concentrations of quinones. An unusual threshold density of quinones (${\Gamma}_c$ = 5.2-7.2%), at which the pseudo-first order rate constant started to vary as the reaction progressed, was observed. This unexpected kinetic behavior was attributed to the phase-separation phenomena of multi-component SAMs. Additional experiments using more phase-separated two-component SAMs supported this explanation by revealing a significant decrease in ${\Gamma}_c$ values. When the background hydroxyl group was replaced with carboxylic or phosphoric acid groups, ${\Gamma}_c$ was observed at below 1%. Also, more phase-separated thermodynamically controlled SAMs produced a lower critical density (3% < ${\Gamma}_c$ < 4.9%) than that of the less phaseseparated kinetically controlled SAMs (6.5% < ${\Gamma}_c$ < 8.9%).

• 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.