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Quinone

About: Quinone is a research topic. Over the lifetime, 5818 publications have been published within this topic receiving 110450 citations. The topic is also known as: quinones.


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Journal ArticleDOI
TL;DR: The higher redox potential benzoquinones and naphthoquinones are the most cytotoxic presumably because of their higher electrophilicty and thiol reactivity and/or because the quinones or GSH conjugates are more readily reduced to semiquinones which activate oxygen.

989 citations

Journal Article
TL;DR: 6-hydroxydopamine and 2,4,5-trihydroxyphenylalanine kill cells through the production of H2O2, O2[unknown], and OH·, while for dopamine and dopa the reaction of quinone oxidation products with nucleophiles probably also contributes to their cytotoxicity.
Abstract: The mechanism of cytotoxicity of 6-hydroxydopamine, 2,4,5-trihydroxyphenylalanine, dopa, dopamine, norepinephrine, and epinephrine was explored by asking whether cytotoxicity was a reflection of the potential for autoxidation of each polyphenol or of the sulfhydryl reactivity of its quinone products. The cytotoxicity of the polyphenols, as measured by inhibition of [3H]thymidine incorporation into DNA by C1300 neuroblastoma cells in tissue culture, correlated with the rate of autoxidation, as measured spectrophotometrically or by oxygen electrode studies. Polarographic determinations of the oxidation potentials of the polyphenols were also predictive of cytotoxicity; the most cytotoxic compounds had the most negative half-wave potentials and thus were the most readily oxidized. By contrast, the sulfhydryl reactivity of the quinone oxidation products of the polyphenols, as measured by inhibition of purified calf thymus DNA polymerase α, exhibited an inverse relationship to the cytotoxicity of the polyphenols; the most toxic compounds, 6-hydroxydopamine and 2,4,5-trihydroxyphenylalanine, were oxidized to the least reactive quinone products. An alternative mechanism of toxicity was observed with N -acetyldopamine, which was oxidized to 4-(2- N -acetylaminoethyl)-1,2-benzoquinone, a potent sulfhydryl reagent. N -Acetyldopamine was more toxic than predicted by its half-wave potential or its rate of autoxidation. Furthermore, while norepinephrine completely neutralized 6-hydroxydopamine and 2,4,5-trihydroxyphenylalanine as cytotoxic agents, the toxicity of N -acetyldopamine was minimally affected. Thus we conclude that 6-hydroxydopamine and 2,4,5-trihydroxyphenylalanine kill cells through the production of H2O2, O2[unknown], and OH·, while for dopamine and dopa the reaction of quinone oxidation products with nucleophiles probably also contributes to their cytotoxicity.

969 citations

Journal ArticleDOI
TL;DR: The sulfate radical pathway of the room-temperature degradation of two phenolic compounds in water is reported, and it provides strong evidence on the interaction of chloride ions with sulfate radicals leading to halogenation of organics in water.
Abstract: The sulfate radical pathway of the room-temperature degradation of two phenolic compounds in water is reported in this study. The sulfate radicals were produced by the cobalt-mediated decomposition of peroxymonosulfate (Oxone) in an aqueous homogeneous system. The major intermediates formed from the transformation of 2,4-dichlorophenol were 2,4,6-trichlorophenol, 2,3,5,6-tetrachloro-1,4-benzenediol, 1,1,3,3-tetrachloroacetone, pentachloroacetone, and carbon tetrachloride. Those resulting from the transformation of phenol in the presence of chloride ion were 2-chlorophenol, 4-chlorophenol, 2,4-dichlorophenol, 2,6-dichlorophenol, 1,1,3,3-tetrachloroacetone, and pentachloroacetone. In the absence of chloride ion, phenol transformed into 2,5-cyclohexadiene-1,4-dione (quinone), 1,2-benzenediol (catechol), and 1,4-benzenediol (hydroquinone). Several parameters were varied, and their impact on the transformation of the organic compounds is also discussed. The parameters varied were the initial concentration of the organic substrate, the dose of Oxone used, the cobalt counteranion, and in particular the impact of chloride ions and the quenching agent utilized for terminating the reaction. This is one of the very few studies dealing with intermediates formed via sulfate radical attack on phenolic compounds. It is also the first studythat explores the sulfate radical mechanism of oxidation, when sulfate radicals are generated via the Co/Oxone reagent. Furthermore, it provides strong evidence on the interaction of chloride ions with sulfate radicals leading to halogenation of organics in water.

808 citations

Journal ArticleDOI
TL;DR: The protective effects of BHA appear to be due, at least in part, to the ability of this antioxidant to increase the activities in rodent tissues of several enzymes involved in the nonoxidative metabolism of a wide variety of xenobiotics.
Abstract: 2(3)-tert-Butyl-4-hydroxyanisole (BHA) is one of several widely used antioxidant food additives that protect against chemical carcinogenesis and toxicity. The present report concerns the enhancement of dicoumarol-inhibited NAD(P)H:quinone reductase [NAD(P)H dehydrogenase (quinone); NAD(P)H:(quinone acceptor) oxidoreductase, EC 1.6.99.2] activity in mouse tissues in response to dietary administration of BHA. Cytosolic quinone reductase specific activity was increased significantly in 10 of 15 tissues examined from BHA-fed mice. The greatest proportionate increase, to 10 times control levels, was observed in liver. BHA also increased the quinone reductase activities of kidney, lung, and the mucosa of the upper small intestine severalfold. The increases of quinone reductase activities in liver and digestive tissues in response to BHA were comparable to the increases previously observed in glutathione S-transferase (EC 2.5.1.18) and epoxide hydratase (EC 3.3.2.3) activities. Quinones are among the toxic products of oxidative metabolism of aromatic hydrocarbons. NAD(P)H:quinone reductase exhibits broad specificity for structurally diverse hydrophobic quinones and may facilitate the microsomal metabolism of quinones to readily excreted conjugates. The protective effects of BHA appear to be due, at least in part, to the ability of this antioxidant to increase the activities in rodent tissues of several enzymes involved in the nonoxidative metabolism of a wide variety of xenobiotics.

757 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023157
2022271
202180
2020121
2019110
201897