Quinone chemistry and toxicity

Monks, Terrence J.; Hanzlik, Robert P.; Cohen, Gerald M.; Ross, David; Graham, Doyle G.

doi:10.1016/0041-008x(92)90273-u

Cited by 696 publications

(431 citation statements)

References 92 publications

Supporting

Mentioning

407

Contrasting

Unclassified

Order By: Relevance

“…The two-electron reduction of the metabolic products of polycyclic aromatic hydrocarbons such as quinones, catalyzed by quinone reductase also known as DT-diaphorase, has been considered to be a detoxification pathway, since the resulting hydroquinones may be conjugated and excreted through mercapturic acid pathways (Monks et al 1992). These quinones in addition to electrophilic characteristics, are well known oxidants (Monks et al 1992) which covalently bind to DNA-forming depurinating adducts and play a definitive role in cancer induction (Cavalieri et al 1997).…”

Section: Discussionmentioning

confidence: 99%

“…These quinones in addition to electrophilic characteristics, are well known oxidants (Monks et al 1992) which covalently bind to DNA-forming depurinating adducts and play a definitive role in cancer induction (Cavalieri et al 1997). The semiquinone, the product of one electron reduction of quinines via microsomal NADPH-cytochrome P-450, may be toxic perse or react with molecular oxygen, forming O 2 and regenerating the parent quinines, which is then available for re-reduction and thereby undergoes a futile redox cycling (Monks et al 1992). The net result of such a redox cycling is an oxidative stress resulting from disproportionate consumption of cellular reducing equivalent and generation of reactive oxygen species such as O 2 , H 2 O 2 and OH (Perchellet & Perchellet 1989;Sun 1990).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

265

147

View full text Add to dashboard Cite

Dietary antioxidants protect laboratory animals against the induction of tumours by a variety of chemical carcinogens. Among possible mechanism of protection against chemical carcinogenesis could be mediated via-antioxidantdependent induction of detoxifying enzymes. Curcumin, a yellow pigment from Curcuma longa, is a major component of turmeric and is commonly used as a spice and food colouring material and exhibits antiinflammatory, antitumour, and antioxidant properties. In this study we therefore investigated the effect of dietary supplementation of curcumin on the activities of antioxidant and phase II-metabolizing enzymes involved in detoxification, and production of reactive oxygen species were quantified in ddY male mice. Dietary supplementation of curcumin (2%, w/v) to male ddY mice for 30 days significantly increased the activities of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and catalase to 189%, 179%, 189%, and 181% in liver and 143%, 134%, 167% and 115% in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.001). Parallel to these changes, curcumin feeding to mice also resulted in a considerable enhancement in the activity of phase II-metabolizing enzymes viz. glutathione S-transferase and quinone reductase to 1.7 and 1.8 times in liver and 1.1 and 1.3 times in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.01). In general, the increase in activities of antioxidant and phase II-metabolizing enzymes was more pronounced in liver as compared to kidney. The induction of such detoxifying enzymes by curcumin suggest the potential value of this compound as protective agent against chemical carcinogenesis and other forms of electrophilic toxicity. The significance of these results can be implicated in relation to cancer chemopreventive effects of curcumin against the induction of tumours in various target organs.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

265

147

View full text Add to dashboard Cite

show abstract

“…Studies using fractionated organic DEP extract have demonstrated that quinones and PAHs are representative organic chemical groups that could contribute to the oxidant injury in the lung [23][24][25]. PAHs can be converted to quinones via biotransformation, e.g.…”

Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

“…through reactions involving cytochrome P450 1A1, expoxide hydrolase and dihydrodiol dehydrogenase [26]. Quinones produce ROS and may be key compounds in PM toxicity along with transition metals [24,26]. Redox cycling quinones undergo one-electron reductions by NADPH cytochrome P450 reductase to form semiquinones [27].…”

Section: Generation Of Oxidative Stress By Ambient Particulate Pollutmentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

800

527

View full text Add to dashboard Cite

Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

show abstract

“…Menadione (MD) is such a drug, generating reactive superoxide ions, which can be further oxidized to give HP (Monks et al, 1992;Shackelford et al, 2000). It has been previously reported that exposure to HP or MD results in a cell cycle arrest (Flattery-O'Brien and Dawes, 1998;Leroy et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Disruption of Yeast Forkhead-associated Cell Cycle Transcription by Oxidative Stress

Shapira

Segal

Botstein

2004

MBoC

View full text Add to dashboard Cite

The effects of oxidative stress on yeast cell cycle depend on the stress-exerting agent. We studied the effects of two oxidative stress agents, hydrogen peroxide (HP) and the superoxide-generating agent menadione (MD). We found that two small coexpressed groups of genes regulated by the Mcm1-Fkh2-Ndd1 transcription regulatory complex are sufficient to account for the difference in the effects of HP and MD on the progress of the cell cycle, namely, G1 arrest with MD and an S phase delay followed by a G2/M arrest with HP. Support for this hypothesis is provided by fkh1fkh2 double mutants, which are affected by MD as we find HP affects wild-type cells. The apparent involvement of a forkhead protein in HP-induced cell cycle arrest, similar to that reported for Caenorhabditis elegans and human, describes a potentially novel stress response pathway in yeast. INTRODUCTIONReactive oxygen species (ROS) are by-products of aerobic metabolism, but are also attributes of the extracellular environment. They pose a threat to organisms by damaging a variety of cellular macromolecules, including DNA, membrane lipids, and proteins and are implicated with carcinogenesis, aging, and numerous degenerative diseases (Finkel and Holbrook, 2000;Neumann et al., 2003). The major ROS derived from oxygen are superoxide ions, hydrogen peroxide (HP), and hydroxy radicals, ordered here by increasing reactivity (reviewed in Shackelford et al., 2000).Oxidative stress in yeast has been studied by exposing cells to agents that are already reactive, typically HP, or drugs that cause the intracellular accumulation of reactive oxygen species (Godon et al., 1998;Dumond et al., 2000;Gasch et al., 2000). Menadione (MD) is such a drug, generating reactive superoxide ions, which can be further oxidized to give HP (Monks et al., 1992;Shackelford et al., 2000). It has been previously reported that exposure to HP or MD results in a cell cycle arrest (Flattery-O'Brien and Dawes, 1998;Leroy et al., 2001). However, the arrest points are not similar for the two agents. MD was reported to arrest cells at the G1 phase of the cell cycle, whereas HP was suggested to cause a G2 arrest by an alternate mechanism from that affected by MD (Flattery-O'Brien and Dawes, 1998); others reported that HP exposure causes a delay in the S phase (Leroy et al., 2001).Hundreds of genes are regulated so that they are expressed at specific times in the cell cycle and not at others (Cho et al., 1998;Spellman et al., 1998). The major part of this coordination is achieved by the sequential activation of a small number of transcription regulators (reviewed in Mendenhall and Hodge, 1998): MBF (a complex of Mbp1p and Swi6p) and SBF (a complex of Swi4p and Swi6p) are responsible for activating G1 transcription (Koch et al., 1993); Fkh1p and a complex formed by the cooperative promoter binding of Mcm1p and Fkh2p and a later recruitment of Ndd1p are responsible for activating G2/M transcription (Koranda et al., 2000;Kumar et al., 2000;Pic et al., 2000;Hollenhorst et al., 2001); Swi5p and Ace2p...

show abstract

Quinone chemistry and toxicity

Cited by 696 publications

References 92 publications

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Disruption of Yeast Forkhead-associated Cell Cycle Transcription by Oxidative Stress

Contact Info

Product

Resources

About