Disease relevance of Flexamine G

• Cultured primary hepatocytes pretreated (protected) with the iron chelator deferoxamine or the antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD) were resistant to the toxicity of 5 microM naphthazarin (5,8-dihydroxy-1,4-naphthoquinone) during a 180-min exposure [1].
• Mercury chloride-induced acute renal failure was also prevented by an antioxidant N,N'-diphenyl-p-phenylenediamine [2].

High impact information on Flexamine G

• We found that the antioxidant N,N'-diphenyl-1,4-phenylenediamine (DPPD) inhibits in vitro LDL oxidation at concentrations much lower than other reported antioxidants [3].
• Pretreatment of the hepatocytes with deferoxamine, a ferric iron chelator, or the addition of the antioxidants N,N'-diphenyl-p-phenylenediamine or catechol prevented the loss of viability [4].
• Activation of the enzyme and lipid peroxidation induced by Fe2+ plus DTT, ascorbic acid, or NADPH was completely prevented by simultaneous addition of N,N'-diphenyl-p-phenylenediamine, an inhibitor of lipid peroxidation [5].
• The oxidative stress could be prevented by inhibition of the beta-lyase-mediated formation and covalent binding to cellular macromolecules of reactive DCVC metabolites, with amino oxyacetic acid (AOA), or by the antioxidant N,N'-diphenyl-p-phenylenediamine [6].
• The voltammetric response of a 10% (by weight) N,N'-diphenyl-p-phenylenediamine (DPPD) and 90% (by weight) carbon and binder screen-printed electrode has been examined in aqueous media over a range of pH using cyclic voltammetry both in the presence and in the absence of sulfide [7].

Chemical compound and disease context of Flexamine G

• Pretreatment of the hepatocytes with the ferric iron chelator deferoxamine or addition to the culture medium of the antioxidant N,N'-diphenyl-p-phenylenediamine prevented the toxicity of acetaminophen in the presence of BCNU whether or not there was acetone in the cultures [8].
• This toxicity was blocked by DPPD or chelating the Fe, but not by glycine [9].
• Effect of different oxygen pressures and N,N'-diphenyl-p-phenylenediamine on Adriamycin toxicity to cultured neonatal rat heart myocytes [10].
• The possibility that lipid peroxidation is involved in valproic acid (VPA) hepatotoxicity was explored by testing the ability of the free-radical scavengers alpha-tocopherol (vitamin E) and N,N'-diphenyl-p-phenylenediamine (DPPD) to protect against VPA toxicity [11].
• Effect of the antioxidant N,N1-diphenyl-p-phenylenediamine (DPPD) on bromobenzene metabolism and toxicity in isolated hepatocytes [12].

Biological context of Flexamine G

• N-Acetyl-L-cysteine, vitamin E, and N,N'-diphenyl-p-phenylenediamine protected against the loss of cell viability [13].
• The antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD) prevented necrosis after IDAM treatment, but the cells went on to die with hallmarks of apoptosis, i.e., cell detachment, caspase-3 activation, cleavage of poly(ADP-ribose)polymerase (PARP), and DNA-ladder formation, all of which were blocked by the general caspase inhibitor zVAD [14].
• The antioxidant, N,N'-diphenyl-p-phenylenediamine (DPPD), which blocked TEPAu-induced malondialdehyde formation but not cell death, also had no effect on the decreases in oxygen consumption, ATP, ATP/ADP ratio, or energy charge [15].
• In addition, the inhibitory effects of the antioxidants and radical scavengers N,N'-diphenyl-p-phenylenediamine (DPPD), (+)-cyanidanol-3 or alpha-tocopherol on CP-induced lipid peroxidation and CP-induced decrease of gluconeogenesis and the inhibitory effect of DPPD on CP-induced decrease of PAH accumulation were evaluated [16].

Anatomical context of Flexamine G

• Injection of the antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD, 0.5 g/kg, i.p.) at 24 h prior to CDDP treatment abolished the increased vulnerability of renal microsomes to lipid peroxidation [17].
• Exposure of U937 cells to the antioxidant 2,6-di-tert-butyl-4-methylphenol (BHT), unlike exposure to other antioxidants such as N,N'-diphenyl-1,4-phenylenediamine, Trolox or alpha-tocopherol, promotes a time- and concentration-dependent induction of apoptosis [18].

Associations of Flexamine G with other chemical compounds

• Pretreatment with the ferric iron chelator deferoxamine or the antioxidant N,N'-diphenyl-1,4-phenylenediamine prevented the loss of ascorbate and the cell killing by TBHP in hepatocytes either sufficient or deficient in alpha-T [19].
• The antioxidant N,N'-diphenyl-1,4-phenylenediamine reduced the loss of alpha-T and significantly decreased lipid peroxidation [20].
• The present experiment was designed to investigate the effect of selenium (Se) supplementation, as sodium selenite, on organic solvent-soluble lipofuscin pigment (OLP) accumulation and glutathione peroxidase (GSH-Px) activity in the livers of mice fed varying levels of vitamin E or N,N'-diphenyl-p-phenylenediamine (DPPD) [21].
• The reactivity toward radicals and antioxidant activity of bisphenol per se were found to be much smaller than those of alpha-tocopherol or N,N'-diphenyl-p-phenylenediamine (DPPD) but stronger than probucol [22].
• Antioxidants, N-acetyl cysteine (NAC) or N,N'-diphenyl-p-phenylenediamine significantly inhibited both the ROI generation and apoptosis [23].

Gene context of Flexamine G

• The antioxidant N,N'-diphenyl-p-phenylenediamine prevented lipid peroxidation and cell death but had no effect on elevated cytosolic Ca2+, delta psi loss, GSH depletion, or G3PD inactivation [24].
• (2) The CrVI-induced lipid peroxidation was inhibited by catalase and mannitol as scavengers of active oxygen species, or N,N'-diphenyl-p-phenylenediamine and alpha-tocopherol as antioxidants [25].
• The effect of age and dietary supplementation of vitamin E or N,N'-diphenyl-p-phenylenediamine (DPPD) on organic solvent-soluble lipofuscin pigments (OLP) and glutathione peroxidase (GSH-Px) activity in mouse heart and brain was investigated [26].
• N,N'-diphenyl-p-phenylenediamine (DPPD), an antioxidant, reduced ROS production induced by serum deprivation and recovered cell survival [27].
• The reactive species generated by light activation of CDS1 were effectively quenched by N,N'-diphenyl-p-phenylenediamine [28].

Analytical, diagnostic and therapeutic context of Flexamine G

• To establish the apoptosis model of the SMMC-7721 hepatocellular carcinoma cell, we treated cells with DCVC in EBSS for different concentrations or for various length times in the presence of 20 micromol/L N,N'-diphenyl-p-phenylenediamine, which blocks necrotic cell death and identified this model by flow cytometry and DNA ladder [29].
• Acute renal failure was induced by subcutaneous injection of mercury chloride (10 mg/kg), and animals were pretreated with JSE (0.1 g/kg, orally) for 7 days or N,N'-diphenyl-p-phenylenediamine (0.5 g/kg, i.p.) 24 h prior to the injection of mercury chloride [2].

References