potassium-ascorbyl-tocopheryl-phosphate has been researched along with 6-hydroxy-2-5-7-8-tetramethylchroman-2-carboxylic-acid* in 4 studies
4 other study(ies) available for potassium-ascorbyl-tocopheryl-phosphate and 6-hydroxy-2-5-7-8-tetramethylchroman-2-carboxylic-acid
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The α-tocopherol derivative ESeroS-GS induces cell death and inhibits cell motility of breast cancer cells through the regulation of energy metabolism.
Cancer cells are known to exhibit different hallmarks compared with normal cells. Therefore, targeting these features may improve the response to cancer therapy. In this study, we provided direct evidence that the α-tocopherol derivative ESeroS-GS inhibited the viability, migration, and invasion of breast cancer cells. ESeroS-GS induced cell death in different cancer cells in a dose-dependent manner but showed no significant effects on MCF-10A mammary epithelial cells. Although the ESeroS-GS-induced cell death in MDA-MB-231 breast cancer cells was accompanied with the generation of reactive oxygen species and the down regulation of mitochondrial membrane potential (MMP), no such effect on reactive oxygen species and MMP was seen in MCF-10A cells. Further studies indicated that ESeroS-GS down-regulated the expression of hexokinase II, SDH B, UQCRC2 and COX II in MDA-MB-231 cells but not in MCF-10A cells. The down-regulation of these enzymes accounts for the decreased oxidative phosphorylation (OXPHOS) and glycolysis in MDA-MB-231 cells upon ESeroS-GS treatment. We also found that sub-toxic concentration of ESeroS-GS treatment resulted in the impairment of F-actin cytoskeleton assembly and the consequently decreased migratory and invasive ability of MDA-MB-231 cells, which might be due to the inhibition of cellular energy metabolism. These results indicate that ESeroS-GS shows potential to become a novel anti-cancer agent by targeting the energy metabolism of cancer cells. Topics: Adenosine Triphosphate; alpha-Tocopherol; Animals; Antineoplastic Agents; Antioxidants; Ascorbic Acid; Benzopyrans; Breast Neoplasms; Cell Line; Cell Line, Tumor; Cell Movement; Cell Survival; Chromans; Dose-Response Relationship, Drug; Energy Metabolism; Female; Glycolysis; HeLa Cells; Humans; Indoles; Mammary Glands, Human; Membrane Potential, Mitochondrial; Mice; Neoplasm Invasiveness; NIH 3T3 Cells; Oxidative Phosphorylation; Reactive Oxygen Species; Vitamin E | 2014 |
Inhibitory effect of antioxidants on hydroxyl radical generation from methylguanidine: an ESR study.
Methylguanidine (MG) is known as not only a nephrotoxin but also as a neurotoxine. We have previously showed that MG itself generates hydroxyl radicals (*OH) in an in vitro study. In this study, we examined the inhibitory effects of ascorbate, EPC-K(1) (alpha-tocopheryl-L-ascorbate-2-O-phosphate diester), Trolox (water-soluble vitamin E analogue), and glutathione (GSH) on *OH generation from MG using an electron spin resonance (ESR) spectrometry with spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). It was found that these compounds have potent inhibitory effect on *OH generation from MG in the order of ascorbate > GSH > EPC-K(1) > Trolox. Topics: Antioxidants; Ascorbic Acid; Chromans; Cyclic N-Oxides; Electron Spin Resonance Spectroscopy; Glutathione; Hydroxyl Radical; Methylguanidine; Spin Trapping; Vitamin E | 2009 |
Novel approach to in vivo screening for radioprotective activity in whole mice: in vivo electron spin resonance study probing the redox reaction of nitroxyl.
Previously, we reported that X-irradiation enhanced the signal decay of a spin probe injected into whole mice measured by in vivo ESR, and that the observed enhancement was suppressed by the pre-administration of cysteamine, a radioprotector [Miura, Y., Anzai, K., Urano, S. and Ozawa, T. (1997) Free Rad. Biol. Med. 23: 533-540]. In the present study, the suppression activity of the X-ray-induced increase in the ESR signal decay rate (termed suppression index, SI) was measured for several radioprotectors: 5-hydroxytryptamine (5-HT), S-2-(3-aminopropylamino)-ethylphosphorothioic acid (WR-2721), 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl (TEMPOL), cimetidine, interleukin-1 beta (IL-1 beta) and stem cell factor (SCF). The enhancement of the ESR signal decay of carbamoyl-PROXYL due to X-irradiation was suppressed by a treatment with all of the radioprotectors examined, showing positive SI values. However, a dose-dependency of 5-HT or WR-2721 was not observed, suggesting that several mechanisms exist for radioprotection and a modification of the signal decay rate. Although the in vivo ESR system cannot be used in place of the 30-day survival method for the assessment of radioprotectors, this system might be applicable to in vivo, non-invasive screening prior to using the 30-day survival method. Topics: Amifostine; Animals; Ascorbic Acid; Chromans; Cimetidine; Cyclic N-Oxides; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Interleukin-1; Mice; Nitrogen Oxides; Oxidation-Reduction; Oxidative Stress; Pyrrolidines; Radiation-Protective Agents; Recombinant Proteins; Serotonin; Spin Labels; Stem Cell Factor; Vitamin E; Whole-Body Irradiation | 2000 |
Antioxidant properties of EPC-K1: a study on mechanisms.
Scavenging effects of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8- tetramethyl-2-(4,8,12-trimethytridecyl)-2H-1-benzopyran- 6-yl-hydrogen phosphate] potassium salt (EPC-K1) on hydroxyl radicals, alkyl radicals and lipid radicals were studied with ESR spin trapping techniques. The inhibition effects of EPC-K1 on lipid peroxidation were assessed by TBA assay. The kinetics of EPC-K1 reacting with hydroxyl radicals and linoleic acid radicals were studied by pulse radiolysis. The active site of EPC-K1 and the structure-antioxidative activity relationships were discussed. The superoxide radicals scavenging capacity of the brain homogenate of EPC-K1-treated rats was measured. The results revealed that in comparison with Trolox and vitamin C, EPC-K1 showed better overall antioxidative capacity in vitro and in vivo. EPC-K1 was a moderate scavenger on hydroxyl radicals and alkyl radicals, a potent scavenger on lipid radicals, and an effective inhibitor on lipid peroxidation. EPC-K1 could react with hydroxyl radicals with a rate constant of 7.1 x 10(8) dm3 mol-1 s-1 and react with linoleic acid radicals with a rate constant of 2.8 x 10(6) dm3 mol-1 s-1. The active site of EPC-K1 was the enolic hydroxyl group. After administration of EPC-K1, the ability of rat brain to scavenge superoxide radicals was significantly increased. The potent scavenging effects of EPC-K1 on both hydrophilic and hydrophobic radicals were relevant with its molecular structure, which consisted of both hydrophilic and hydrophobic groups. Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Chromans; Electron Spin Resonance Spectroscopy; Free Radical Scavengers; Hydroxyl Radical; Linoleic Acid; Lipid Peroxidation; Male; Molecular Structure; Peroxides; Pulse Radiolysis; Rats; Rats, Wistar; Spectrophotometry; Structure-Activity Relationship; Vitamin E | 1999 |