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F: The antitumor ether lipid ET-18-OCH(3) induces apoptosis through translocation and capping of Fas/CD95 into membrane rafts in human leukemic cells. Blood 2001,98(13):3860–3863.PubMedCrossRef 69. Ayllon V, Fleischer A, Cayla X, Garcia A, Rebollo A: Segregation of Bad from lipid rafts is implicated in the induction of apoptosis. J Immunol 2002,168(7):3387–3393.PubMed 70. Thomas BJ, Rothstein R: Elevated recombination rates in transcriptionally active DNA. Cell 1989,56(4):619–630.PubMedCrossRef 71. Sherman F: Getting started with yeast. Methods Enzymol. 2002, 350:3–41. 72. Guaragnella N, Pereira C, Sousa MJ, Antonacci L, Passarella S, Corte-Real M, ISRIB Marra E, Giannattasio S: YCA1 participates in the acetic acid induced yeast programmed cell death also in a manner unrelated to its caspase-like activity. FEBS Lett 2006,580(30):6880–6884.PubMedCrossRef Authors’ contributions JT and FF-O carried out the experimental studies, having contributed 75% and 25% respectively. CF supervised JT and FF-O and checked the data. JT and CF wrote this manuscript. CL revised the manuscript. All authors read and approved the final manuscript.”
“Background Hydrogen peroxide (H2O2) and

hypochlorous acid (HOCl) are reactive oxygen species that are part of the oxidative burst encountered by S. Typhimurium upon internalization by phagocytic cells. Under acidic conditions, such as those found inside the Mannose-binding protein-associated serine protease phagosome, H2O2 is generated spontaneously by the reaction of two superoxide anion (O2 −) molecules [1]. Moreover, S. Typhimurium encodes both periplasmic and cytoplasmic superoxide dismutases that catalyze O2 − dismutation to generate H2O2 and molecular oxygen [2–4]. HOCl is produced by the action of myeloperoxidase (MPO) in a reaction that depends on H2O2, Cl−and acidic conditions [5, 6]. Taken together, H2O2 and HOCl react with thiol and heme groups, copper and iron salts generating the reactive hydroxyl radical (OH.). As a consequence, they produce lipid peroxidation, chlorination of tyrosine residues, oxidation of iron centers, protein cross linking and DNA damage [5–8].

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