In solution stability of organic peroxides

<p>Organic peroxides are compounds possessing one or more oxygen–oxygen bonds. They are derivatives of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), in which one or both hydrogens are replaced by a group containing carbon. This kind of compounds are ubiquitous in the environment being detected in Secondary Organic Aerosols (SOA)<sup>1,2</sup>, rainwater, and cloud water<sup>3,4</sup>. The role of peroxides is very important from health and climate perspectives<sup>5</sup>, and to understand the mechanism of SOA formation<sup>6</sup>. It is known that they can easily decompose to form H<sub>2</sub>O<sub>2</sub> and other products<sup>7</sup>. However, the decomposition processes for organic peroxides have not been studied in a systematic way that allow to stablish improved strategies for sampling and storage of the samples. Moreover, these processes would happen in the atmosphere and need to be included in atmospheric models.</p><p>The aim of this work is to study the decomposition rate at different temperatures of hydroperoxides formed in the aqueous solution of some atmospherically relevant organic compounds with ozone. Iodometric method is used to monitor the total peroxides concentration. The implications related to sampling and storage for atmospheric samples containing organic peroxides are discussed together with the atmospheric impact of the studied processes. <strong>     </strong></p><p><strong>REFERENCES:    1. </strong>Mutzel, A., L. Poulain, T. Berndt, Y. Iinuma, M. Rodigast, O. Böge, S. Richters, G. Spindler, M. Sipila, T. Jokinen, et al. 2015. Environ. Sci. Technol. <strong>2015</strong>, 49 (13):7754–61. ; 2. Kristensen, K., Å. K. Watne, J. Hammes, A. Lutz, T. Petäjä, M. Hallquist, M. Bilde, and M. Glasius. Environ. Sci. Technol. Lett. <strong>2016</strong>, 3 (8):280–5; 3. Kelly, T.J., Daum, P.H. and S.E. Schwartz. J. Geophysical Research. <strong>1985</strong>, 90(D5), 7861-7871; 4. Huang, S., Fuse, Y., Yamda, E. and Kagaku, B. Bunseki Kagaku. <strong>2004,</strong> 53(9), 875-881; 5. Tao, F.; Gonzalez-Flecha, B.; Kobzik, L. Free Radical Biol. Med. <strong>2003</strong>, 35, 327−340; 6.Seinfeld, J. H.; Pandis, S. N. Atmospheric Chemistry and Physics: From Air Pollution to Climate Change, 3rd ed.; John Wiley & Sons: Hoboken, NJ, 2016; 7. Badali, K.M., Zhou, S., Aljawhary, D., Antiñolo, M., Chen, W.J., Lok, A., Mungall, Wong, E., J. P. S., Zhao, R. and Abbatt, J.P.D. Atmos. Chem. Phys., <strong>2015,</strong> 15, 7831–7840.</p>

Relocalized redox-active lysosomal iron is an important mediator of oxidative-stress-induced DNA damage

Oxidative damage to nuclear DNA is known to involve site-specific Fenton-type chemistry catalysed by redox-active iron or copper in the immediate vicinity of DNA. However, the presence of transition metals in the nucleus has not been shown convincingly. Recently, it was proposed that a major part of the cellular pool of loose iron is confined within the acidic vacuolar compartment [Yu, Persson, Eaton and Brunk (2003) Free Radical Biol. Med. 34, 1243–1252; Persson, Yu, Tirosh, Eaton and Brunk (2003) Free Radical Biol. Med. 34, 1295–1305]. Consequently, rupture of secondary lysosomes, as well as subsequent relocation of labile iron to the nucleus, could be an important intermediary step in the generation of oxidative damage to DNA. To test this concept we employed the potent iron chelator DFO (desferrioxamine) conjugated with starch to form an HMM-DFO (high-molecular-mass DFO complex). The HMM-DFO complex will enter cells only via fluid-phase endocytosis and remain within the acidic vacuolar compartment, thereby chelating redox-active iron exclusively inside the endosomal/lysosomal compartment. Both free DFO and HMM-DFO equally protected lysosomal-membrane integrity against H2O2-induced oxidative disruption. More importantly, both forms of DFO prevented H2O2-induced strand breaks in nuclear DNA, including telomeres. To exclude the possibility that lysosomal hydrolases, rather than iron, caused the observed DNA damage, limited lysosomal rupture was induced using the lysosomotropic detergent O-methyl-serine dodecylamine hydrochloride; subsequently, hardly any DNA damage was found. These observations suggest that rapid oxidative damage to cellular DNA is minimal in the absence of redox-active iron and that oxidant-mediated DNA damage, observed in normal cells, is mainly derived from intralysosomal iron translocated to the nucleus after lysosomal rupture.

Thioredoxin peroxidases can foster cytoprotection or cell death in response to different stressors: over- and under-expression of thioredoxin peroxidase in Drosophila cells

Recently, we identified a set of five genes constituting the peroxiredoxin gene family in Drosophila melanogaster [Radyuk, Klichko, Spinola, Sohal and Orr (2001) Free Radical Biol. Med. 31, 1090–1100]. This set includes two abundant thioredoxin peroxidase (TPx) species, namely Drosophila peroxiredoxin DPx-4783, a cytosolic TPx and DPx-5037, a mitochondrial TPx. Overexpression of either one of them in Drosophila S2 cells conferred increased resistance to toxicity induced by hydrogen peroxide, paraquat or cadmium. To understand further the functional roles of these enzymes in vivo, we report in the present study the effects of decreased expression, using RNA interference, on the response of S2 cells to different stressors. When either of the TPxs was blocked, cells became relatively more susceptible to oxidative stress caused by exposure to hydrogen peroxide or paraquat, but were unaffected when challenged with copper and heat stress. In contrast, TPx overexpressing cells were more susceptible to copper and heat stress when compared with control cells and exhibited DNA fragmentation. Furthermore, when cells were supplemented with N-acetyl-l-cysteine together with copper, there was a clear negative effect on cell survival, which was exacerbated by TPx overexpression. Manipulations in the levels of TPxs demonstrated that, under different stress conditions, these enzymes might have both beneficial and detrimental effects on Drosophila cell viability.

Protection by pantothenol and beta-carotene against liver damage produced by low-dose gamma radiation.

Rats were exposed to a total dose of 0.75 Gy of gamma radiation from a 60Co source, receiving three doses of 0.25 Gy at weekly intervals. During two days before each irradiation, the animals received daily intragastric doses of 26 mg pantothenol or 15 mg beta-carotene per kg body mass. The animals were killed after the third irradiation session, and their blood and livers were analyzed. As found previously (Slyshenkov, V.S., Omelyanchik, S.N., Moiseenok, A.G., Trebukhina, R.V. & Wojtczak, L. (1998) Free Radical Biol. Med. 24, 894-899), in livers of animals not supplied with either pantothenol or beta-carotene and killed one hour after the irradiation, a large accumulation of lipid peroxidation products, as conjugated dienes, ketotrienes and thiobarbituric acid-reactive substances, could be observed. The contents of CoA, pantothenic acid, total phospholipids, total glutathione and GSH/GSSG ratio were considerably decreased, whereas the NAD/NADH ratio was increased. All these effects were alleviated in animals supplied with beta-carotene and were completely abolished in animals supplied with pantothenol. In the present paper, we extended our observations of irradiation effects over a period of up to 7 days after the last irradiation session. We found that most of these changes, with the exception of GSH/GSSG ratio, disappeared spontaneously, whereas supplementation with beta-carotene shortened the time required for the normalization of biochemical parameters. In addition, we found that the activities of glutathione reductase, glutathione peroxidase, catalase and NADP-dependent malate (decarboxylating) dehydrogenase ('malic enzyme') in liver were also significantly decreased one hour after irradiation but returned to the normal level within 7 days. Little or no decrease in these activities, already 1 h after the irradiation, could be seen in animals supplemented with either beta-carotene or pantothenol. It is concluded that pantothenol is an excellent radioprotective agent against low-dose gamma radiation.

Protective effect of pantothenic acid and related compounds against permeabilization of Ehrlich ascites tumour cells by digitonin.

Preincubation of Ehrlich ascites tumour cells with millimolar concentrations of pantothenic acid, pantothenol or pantethine, but not with homopantothenic acid, at 22 degrees C or 32 degrees C, but not at 0 degrees C, makes the plasma membrane more resistant to the damaging effect of submillimolar concentrations of digitonin. It is proposed that this increased resistance is due to the increased rate of cholesterol biosynthesis. In fact, incorporation of [14C]acetate into cholesterol is by 45% increased in the cells preincubated with pantothenic acid; this probably reflects elevation of the content of CoA in such cells [Slyshenkov, V.S., Rakowska, M., Moiseenok, A.G. & Wojtczak, L. (1995) Free Radical Biol. Med. 19, 767-772].