muconaldehyde has been researched along with quinone* in 3 studies
3 other study(ies) available for muconaldehyde and quinone
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Benzene metabolites enhance reactive oxygen species generation in HL60 human leukemia cells.
Benzene is myelotoxic and leukemogenic in humans. The mechanisms leading to these effects, however have not been fully elucidated. One of the underlying mechanisms is believed to be the oxidative damage caused by its metabolites. A comparative study was undertaken to examine the relationships between reactive oxygen species (ROS) production, lipid peroxidation and subsequent cytotoxicity induced by five major benzene metabolites. The generation of ROS by benzene metabolites was demonstrated by the significant and dose-dependent increase of intracellular ROS formation in HL60 human promyelocytic leukemia cells in vitro. 1,4-Benzoquinone (BQ) was found to be the most potent metabolite in induction of ROS formation, followed by 1,2,4-benzenetriol (BT) and to a lesser extent, phenol (PH) and trans, trans-muconaldehyde (MD). No significant effect was observed when the cells were treated with trans, trans-muconic acid (MA). The enhancement of ROS production by BQ was effectively inhibited by the addition of catalase, deferoxamine (DFO) and dimethyl sulfoxide (DMSO), but unchanged by superoxide dismutase (SOD), suggest that hydrogen peroxide (H2O2) and hydroxyl radicals (OH) are the two major forms of ROS involved. The results also demonstrate that the ability of benzene metabolites in enhancing ROS generation is closely correlated to their capacity in causing lipid peroxidation and subsequent cytotoxicity. These findings together with earlier parallel observations on DNA damage suggest that ROS play an important role in the mechanism of carcinogenesis induced by benzene metabolites. Topics: Aldehydes; Benzene Derivatives; Benzoquinones; Carcinogens; Catalase; Deferoxamine; Dimethyl Sulfoxide; Dose-Response Relationship, Drug; Free Radical Scavengers; HL-60 Cells; Humans; Hydrogen Peroxide; Hydroquinones; Hydroxyl Radical; Lipid Peroxidation; Phenols; Reactive Oxygen Species; Sorbic Acid; Structure-Activity Relationship; Superoxide Dismutase | 1996 |
Depression of iron uptake into erythrocytes in mice by treatment with the combined benzene metabolites p-benzoquinone, muconaldehyde and hydroquinone.
Using radio-iron uptake into erythrocytes as a measure of hematopoiesis, it was demonstrated that p-benzoquinone (BQ) and muconaldehyde (MUC) are potent inhibitors of bone marrow function in female mice. These two benzene metabolites reduced iron uptake at dosages of less than 5-6 mg kg-1. The combination of MUC and hydroquinone (HQ) (100 mg kg-1) was additive, reducing iron incorporation to an extent that was the sum of the effect of each chemical given alone. The combined effect of MUC and BQ was significantly less than additive, demonstrating antagonism in the response. Multiple regression was used to study the contributions of the components of binary mixtures of the benzene metabolites (METAB). Data obtained from standard curves of METAB and their mixtures are separable in regression analysis. Thus, for zero interaction of METAB, the responses would be simply additive, while positive and negative interaction would indicate synergy and antagonism, respectively. T-testing of the data resulted in non-significant values for the mixture MUC + HQ, indicating zero interaction and an additive response. The negative t-values obtained for the mixture MUC + BQ, however, indicate negative interaction or an antagonistic response. Since mutually exclusive agents share the same binding sites and occupation of a site by one agent excludes its occupation by another, they cannot interact in producing the effect; combinations of these agents show zero interaction and are simply additive. This suggests that HQ and MUC are mutually exclusive and share the same binding site.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Aldehydes; Animals; Benzoquinones; Binding Sites; Depression, Chemical; Drug Synergism; Erythrocytes; Female; Hydroquinones; Iron; Mice | 1991 |
Studies on the mechanism of benzene toxicity.
Using the 59Fe uptake method of Lee et al. it was shown that erythropoiesis in female mice was inhibited following IP administration of benzene, hydroquinone, p-benzoquinone, and muconaldehyde. Toluene protected against the effects of benzene. Coadministration of phenol plus either hydroquinone or catechol resulted in greatly increased toxicity. The combination of metabolites most effective in reducing iron uptake was hydroquinone plus muconaldehyde. We have also shown that treating animals with benzene leads to the formation of adducts of bone marrow DNA as measured by the 32P-postlabeling technique. Topics: Aldehydes; Animals; Benzene; Benzoquinones; Bone Marrow; Catechols; DNA; Drug Interactions; Female; Hydroquinones; Iron Radioisotopes; Mice; Phenol; Phenols; Quinones; Rats; Toluene | 1989 |