Desferrioxamine cell culture

Cell culture Damage to small intestinal epithelial cells by XO can be prevented by SOD and desferrioxamine (Ma et al., 1991), whilst that to rat enterocytes, CaCo cells or rabbit colonic epithelial cells by XO can be decreased by catalase (Baker and Baker, 1990 Baker and Campbell, 1991 Kawabe etal., 1992). 

A comparative kinetic analysis of IRPl activation by NO and H2O2 in culture cells yielded the unexpected outcome that NO, unlike H2O2, elicits a slow activation of IRPl which, in kinetic terms rather resembles responses to iron starvation [136], Furthermore, iron starvation and NO result in a slow induction of both IRPl and IRP2, while H2O2 exclusively activates IRPl with rapid kinetics [126, 136]. IRPl induction by H2O2 is biphasic, in contrast to the effects of iron starvation and NO. While the iron chelator desferrioxamine and NO need to be continuously present for IRPl activation, the presence of H2O2 (at a minimal threshold eoncentration of 10 pm) is only required for 10-15 minutes, and then the activation of IRPl can be completed in the absence of the effector [136, 142]. 

Pre-treatment with desferrioxamine protected human fibroblast (cell line GM 05757) monolayer cultures from cytotoxicity and genotoxicity (singlestrand breaks) induced by the pentachlorophenol (PGP) metabolite, tetrachlorohydroquinone (Witte et al. 2000). Similar pattern of protection were also observed for three other hydroxamic acids aceto-, benzo-, and salicylhydroxamic acid. Dimethylsulphoxide, an efficient hydroxyl radical scavenger, provided only partial protection even at high concentrations. In vitro studies showed that... 

In contrast to many studies that identify beneficial effects of dietary flavonoids against cellular Hpid oxidation, the action of flavonoids on bovine leukemia virus-transformed lamb fibroblasts (line FLK) and HL-60 cells was accompanied by lipid peroxidation [90]. Their toxicity was partly prevented by iron chelator desferrioxamine and antioxidant AA iphenyl-p-phenylene diamine, a result that pointed to the involvement of oxidative stress in their cytotoxicity. Interestingly, the toxicity of quercetin was partly prevented by nontoxic concentrations of other flavonoids examined, thus suggesting potential neutralization of quercetin cytotoxicity by intake of flavonoid mixtures. In another study, supplementation of rat hepatocyte cultures with the flavonoid myricetin led to the formation of phenoxyl radical intermediates, as detected in intact cells by electron paramagnetic resonance (EPR) spectroscopy [220]. These phenoxyl radicals corresponded to one-electron oxidation products of... 

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