Exsperimental details S13 Scheme S1. Schematic diagram for the synthesis of C60-Py S4 Scheme S2. Schematic diagram for the synthesis of C60-I S4 Scheme S3. Schematic diagram for the synthesis of C60-II S6 Scheme S4. Schematic diagram for the synthesis of C60-III S8 Scheme S5. Schematic diagram for the synthesis of C60-IV S11

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Four derivatives of fullerene C60 with covalently bonded simple phenols were tested as inhibitors of oxidation of polyethylene at elevated temperatures 150–250 °C under non-isothermal conditions.

Curcumin, a phytochemical present in the spice named turmeric, and one of the promising anti-aging factors, is itself able to induce cellular senescence. We have recently shown that cells building the vasculature senesced as a result of curcumin treatment. Curcumin-induced senescence was DNA damage-independent; however, activation of ATM was observed. Moreover, neither increased ROS production, nor even ATM were indispensable for senescence progression. In this paper we tried to elucidate the mechanism of curcumin-induced senescence. We analyzed the time-dependence of the level and activity of numerous proteins involved in senescence progression in vascular smooth muscle cells and how inhibition p38 or p38 together with ATM, two proteins involved in canonical signaling pathways, influenced cell senescence. We showed that curcumin was able to influence many signaling pathways of which probably none was dominant and sufficient to induce senescence by itself. However, we cannot exclude that the switch between initiation and progression of senescence is the result of the impact of curcumin on signaling pathways engaging AMPK, ATM, sirtuin 1 and p300 and on their reciprocal interplay. Cytostatic concentration of curcumin induced cellular stress, which exceeded the adaptive response and, in consequence, led to cellular senescence, which is triggered by time dependent activation of several signaling pathways playing diverse roles in different phases of senescence progression. We also showed that activity of β-glucuronidase, the enzyme involved in deconjugation of the main metabolites of curcumin, glucuronides, increased in senescent cells. It suggests a possible local elevation of curcumin concentration in the organism.Electronic supplementary materialThe online version of this article (10.1007/s10522-019-09825-2) contains supplementary material, which is available to authorized users.

In 1923, Wieland and Wingler reported that in the molecular hydrogen producing reaction of hydrogen peroxide with formaldehyde in basic solution, free hydrogen atoms (HC) are not involved. They postulated that bis(hydroxymethyl)peroxide,HOCH 2 OOCH 2 OH, is the intermediate,whichdecomposes to yield H 2 and formate,p roposing am echanismt hat would nowadays be considered as a"concerted process". Since then, several other (conflicting) "mechanisms" have been suggested. Our NMR and Raman spectroscopic and kinetic studies,particularly the determination of the deuterium kinetic isotope effect (DKIE), nowconfirm that in this base-dependent reaction, both Ha toms of H 2 derive from the CH 2 hydrogen atoms of formaldehyde,a nd not from the OH groups of HOCH 2 OOCH 2 OH or from water.Q uantum-chemical CBS-QB3 and W1BD computations show that H 2 release proceeds through ac oncerted process,w hich is strongly accelerated by double deprotonation of HOCH 2 OOCH 2 OH, thereby ruling out afree radical pathway. Angewandte ChemieCommunications Angewandte Chemie Communications 9147