Investigation of Ethyl Radical Quenching by Phenolics and Thiols in Model Wine

Laurie, VF (Felipe Laurie, V.). Univ Talca, Fac Ciencias Agr, Talca, Chile.In the present study, the reaction between 1-hydroxyethyl radicals (1-HER) and various wine-related phenolics and thiols, including gallic acid, caffeic acid, ferulic acid, 3-mercaptohexan-1-ol (3MH), cysteine (Cys), and glutathione (GSH), was studied using competitive spin trapping with electron paramagnetic resonance (EPR) and mass spectrometry. Previous studies have reported several important reactions occurring between quinones and other wine components, but the fate of 1-HER within the context of wine oxidation is less understood. Furthermore, the ability of these compounds to prevent formation of acetaldehyde, a known nonenzymatic oxidation product of ethanol, was measured. The hydroxycinnamic acids and thiol compounds tested at 5 mM concentrations significantly inhibited spin adduct formation, indicating their reactivity toward 1-HER. In addition, we confirm that loss of 3MH under model wine conditions is due to quinone trapping as well as 1-HER-induced oxidation

Removal of fumonisin B1 and B2 from model solutions and red wine using polymeric substances

Fumonisins are a group of mycotoxins found in various foods whose consumption is known to be harmful for human health. In this study, we evaluated the ability of three polymers (Polyvinylpolypyrrolidone, PVPP,; a resin of N-vinyl-2-pyrrolidinone with ethylene glycol dimethacrylate and triallyl isocyanurate, PVP-DEGMA-TAIC; and poly(acrylamide-co-ethylene glycol-dimethacrylate), PA-EGDMA) to remove fumonisin B-1 (FB1) and fumonisin B-2 (FB2) from model solutions and red wine. Various polymer concentrations (1, 5 and 10 mg mL(-1)) and contact times (2, 8 and 24 h) were tested, with all polymers exhibiting fumonisin removal capacities (monitored by LC-MS). The impact of all polymers on polyphenol removal was also assessed. PA-EGDMA showed to be the most promising polymer, removing 71% and 95% of FB1, and FB2, respectively, with only a 22.2% reduction in total phenolics

Multidrug-resistant tumor cells remain sensitive to a recombinant interleukin-4-Pseudomonas exotoxin, except when overexpressing the multidrug resistance protein MRP1

Tumor cells may become resistant to conventional anticancer drugs through the occurrence of transmembrane transporter proteins such as P-glycoprotein (ABCB1), breast cancer resistance protein (ABCG2), or members of the multidrug resistance-associated protein family (MRP1¿MRP5; ABCC1¿ABCC5). In this report, we studied whether tumor cells that are cytostatic drug resistant because of overexpression of one of the above mentioned proteins are sensitive to a new anticancer agent, interleukin-4 toxin (IL-4 toxin). IL-4 toxin is a fusion protein composed of circularly permuted IL-4 and a truncated form of Pseudomonas exotoxin (PE) [IL-4(38¿37)-PE38KDEL]. Ninety-six-h cytotoxicity assays and 10-day clonogenic assays showed that drug-selected multidrug resistant (MDR) tumor cells that overexpress P-glycoprotein or breast cancer resistance proteins are still sensitive to IL-4 toxin. Also, tumor cells transfected with cDNA for MRP2¿5 showed no resistance, or marginal resistance, only to the toxin as compared with the parent cells. In contrast, MRP1-overexpressing cells, both drug selected and MRP1 transfected, are clearly resistant to IL-4 toxin with resistance factors of 4.3 to 8.4. MRP1-overexpressing cells were not resistant to PE itself. IL-4 toxin resistance in MRP1-overexpressing cells could be reversed by the MRP1 inhibitors probenecid or MK571 and were not affected by glutathione depletion by DL-buthionine-S,R-sulfoximine. In a transport assay using plasma membrane vesicles prepared from MRP1-overexpressing cells, IL-4 toxin and IL-4, but not PE, inhibited the translocation of the known MRP1 substrate 17ß-estradiol 17-(ß-D-glucuronide) (E217ßG). These data suggest that MRP1-overexpressing cells are resistant to IL-4 toxin because of extrusion of this agent by MRP1. Still, the results of this study demonstrate that IL-4 toxin effectively kills most MDR tumor cells and, therefore, represents a promising anticancer drug