Disease relevance of Cumyl hydroperoxide

• We have expressed the Arabidopsis 1-Cys Prx AtPER1 in Escherichia coli and show that this protein has antioxidant activity in vitro and protects E. coli in vivo against the toxic oxidant cumene hydroperoxide [1].
• The increased cumene hydroperoxide-induced PUFA oxidation in +FO RBCs was accompanied by a lesser extent of hemolysis [2].
• BZP, TBPB and TBIBHP exhibited significant increases in all three biomarkers associated with tumor promoting activity, CHP produced increases only in sustained epidermal hyperplasia and dermal inflammation, MEKP and DCP produced increases only in sustained epidermal hyperplasia and TBEC produced an increase only in dermal inflammation [3].
• In the present study, we have demonstrated that adenoviral-mediated over-expression of cyclophilin A in rat cortical neuronal cultures can protect neurons from oxidative stress (induced by cumene hydroperoxide) and in vitro ischemia (induced by oxygen glucose deprivation) [4].
• We have studied the effects of plasma and of cumene hydroperoxide (CUM) on adenosine diphosphate ribosyl transferase (ADPRT) from mononuclear leukocytes (HML) of patients with colonic adenomatous polyps (n = 22), with colonic hyperplastic polyps (n = 5) and with neither type of polyp (controls) (n = 6) [5].

High impact information on Cumyl hydroperoxide

• Unlike protection against cumene hydroperoxide, protection afforded by ahpC against RNI was independent of the reducing flavoprotein, AhpF [6].
• The transfected cell lines also had increased peroxidase activity using cumene hydroperoxide as the substrate (1.9- to 3.8-fold) which is consistent with the intrinsic peroxidase activity of alpha class GSTs [7].
• Using electron paramagnetic resonance, radicals were detected after addition of arachidonic acid or cumene hydroperoxide to the microsomal preparation [8].
• Unlike the latter reactions, the microsomal N-oxidation of MAB was independent of cytochrome P-450, as shown by its lack of sensitivity to inhibition by 2-[(2,4-dichloro-6-phenyl)phenoxy]ethylamine and its inability to utilize cumene hydroperoxide in place of reduced pyridine nucleotides and oxygen [9].
• Elevating the gene dosage of GRX1 or GRX2 increases resistance to hydroperoxides including hydrogen peroxide, tert-butyl hydroperoxide and cumene hydroperoxide [10].

Chemical compound and disease context of Cumyl hydroperoxide

• A Bacillus subtilis sigM null mutant, lacking the extracytoplasmic function sigma(M) protein, was sensitive to paraquat (PQ), a superoxide-generating reagent, but not to the redox stress-inducing compounds hydrogen peroxide, cumene hydroperoxide, t-butyl hydroperoxide, or diamide [11].
• Escherichia coli devoid of glutathione (because of transposon insertions in the gshA gene) has normal resistance to H2O2, cumene hydroperoxide, heat, or ionizing radiation [12].
• Like AhpC, cloned DirA reduced the susceptibility of an Escherichia coli ahp mutant to cumene hydroperoxide, suggesting that DirA has alkyl hydroperoxide reductase activity [13].
• Moreover, IdB 1016 at the concentration which completely prevented MDA formation also protected isolated hepatocytes against the toxicity of pro-oxidant agents such as allyl alcohol, cumene hydroperoxide and bromotrichloromethane, without interfering with the activation mechanism of these xenobiotics [14].
• The organic hydroperoxides t-butyl hydroperoxide, cumene hydroperoxide, and peracetic acid were found to act similarly to hydrogen peroxide in causing inactivation of enzymes within intact spores of bacillus megaterium ATCC 19213 concomitant with mortality [15].

Biological context of Cumyl hydroperoxide

• Effect of oxidative stress, produced by cumene hydroperoxide, on the various steps of protein synthesis. Modifications of elongation factor-2 [16].
• Cumene hydroperoxide does not facilitate either hydroxylation and no lipid peroxides can be detected in the system either prior to or after incubation with the substrate [17].
• Cellular growth kinetics and rates of [3H]thymidine incorporation showed that both transfectants were more resistant to oxidative shocks mediated by cumene hydroperoxide or singlet oxygen generated by photosensitized rose bengal than were T47D cells and control transfectants [18].
• Cumene hydroperoxide-mediated inactivation of cytochrome P450 2B1. Identification of an active site heme-modified peptide [19].
• Interaction between non-heme iron of lipoxygenases and cumene hydroperoxide: basis for enzyme activation, inactivation, and inhibition [20].

Anatomical context of Cumyl hydroperoxide

• Depending on the cofactor used, microsomal enzymes catalyzed reductions and/or oxidations of the estrogens: Phenobarbital-induced rat liver microsomes catalyzed the oxidation of DES to 4',4"-diethylstilbestrol quinone (DES quinone) with cumene hydroperoxide as cofactor [21].
• Ultrastructural observations of both UVB- and CUH-treated cells showed a normal morphology of the plasma membranes and intracellular organelles [22].
• The effect of melatonin and its precursor N-acetylserotonin was studied in a model of lipid peroxidation induced in human red blood cells by incubation with cumene hydroperoxide (CHP) and H2O2 [23].
• We observed that although it strongly inhibits the iron-induced lipoperoxidation on mitochondria (IC50 = 1 microM), it shows no protection against an organic oxidant, cumene hydroperoxide [24].
• To this end ventricle membranes, field-stimulated rat left atria and field-stimulated rat right ventricle strips were exposed to 0.1 mM cumene hydroperoxide for 20 min [25].

Associations of Cumyl hydroperoxide with other chemical compounds

• Tertiary peroxyl radicals were directly detected by ESR from incubations of tert-butyl hydroperoxide or cumene hydroperoxide with chloroperoxidase at pH 6 [26].
• The level of pgr1(+) transcripts increased by treatment with oxidants such as menadione, cumene hydroperoxide, and diamide [27].
• The overexpressed product of the gene was confirmed to have GST activity toward 1-chloro-2,4-dinitrobenzene and ethacrynic acid and GSH-dependent peroxidase activity toward cumene hydroperoxide [28].
• Monomeric P-450LM2 formed with 20 mM CHAPS catalyzed the hydroxylation of toluene by cumene hydroperoxide [29].
• However NADPH-dependent lipid peroxidation and the cumene hydroperoxide have been found to inactivate placental mitochondrial cytochrome P-450SCC [30].

Gene context of Cumyl hydroperoxide

• Both GST D1 and GST D21 have similar levels of GSH peroxidase activity against cumene hydroperoxide [31].
• A significant increase (1.2-fold) was also observed in GPX activity toward cumene hydroperoxide, but CAT and SOD activities remained unchanged [32].
• When OR was bypassed and the hydroxylation was supported by cumene hydroperoxide, no difference in the rates of diclofenac 4'-hydroxylation was observed for CYP2C9 and the R144C variant regardless of OR to P450 ratio [33].
• Kidney GPx activities were significantly affected; activity assayed with cumene hydroperoxide (cu-OOH) was increased but activity assayed with H2O2 was reduced [34].
• On the other hand, a slight initial increase in the GPO activity with cumene hydroperoxide was followed by a return to control values, and the GPO activity with H2O2 was decreased only slightly with time [35].

Analytical, diagnostic and therapeutic context of Cumyl hydroperoxide

• Cardioplegia induced a 41% (P = .08) decrease in rat heart MDA content, whereas cumene hydroperoxide increased it 3.6 times (P < .01) [36].
• Since the enzyme retains catalytic activity, albeit diminished, after treatment with cumene hydroperoxide, the structure of the iron site may reflect the catalytically relevant form of the cofactor [20].
• Neonatal rat heart cell cultures were subjected to a standardized protocol of oxidative stress using 80 mumol.l-1 cumene hydroperoxide (CHPO) for 0-90 min [37].
• This was effected by autoxidation, by cumene hydroperoxide (with GSH peroxidase) and by titration with N-ethylmaleimide (NEM) [38].
• Oxidation of specific phospholipid classes was measured in normal human epidermal keratinocytes exposed to cumene hydroperoxide after metabolic incorporation of the fluorescent oxidation-sensitive fatty acid, cis-parinaric acid, using a fluorescence high-performance liquid chromatography assay [39].

References