@misc{BraudBussMerteetal., author = {Braud, Nicolas and Buß, Lars and Merte, Lindsay Richard and Wallander, Harald and Krisponeit, Jon-Olaf and Schmidt, Thomas and Lundgren, Edvin and Flege, Jan Ingo and Falta, Jens}, title = {Growth and oxidation of ultra-thin Pt-Sn layers on Pt(111) by molecular and atomic oxygen}, series = {Ultramicroscopy}, volume = {278}, journal = {Ultramicroscopy}, publisher = {Elsevier BV}, address = {Amsterdam}, issn = {0304-3991}, doi = {10.1016/j.ultramic.2025.114243}, pages = {1 -- 11}, abstract = {The preparation of ultra-thin PtSn-alloyed layers by molecular beam epitaxy was studied using low-energy electron microscopy (LEEM) and micro-diffraction (-LEED). Deposition at a sample temperature of 435 °C initially results in the formation of a PtSn/Pt(111) layer showing a (2 × 2) reconstruction. With continued Sn deposition, a PtSn/Pt(111) layer develops, showing a ()R30° reconstruction. An ultra-thin tin oxide was formed from the (2 × 2) surface by exposure to molecular oxygen at temperatures of 500 °C and 590 °C, respectively. LEED shows the evolution of a new surface structure, which could be identified as an incommensurate rectangular reconstruction with lattice parameters of a = (6.4 ± 0.1) {\AA} and b = (8.6 ± 0.1) {\AA} present in three domains rotated by 120° with respect to each other. This structure can be related to the zigzag reconstructions found for similar ultra-thin oxide systems. Contrarily, the ()R30° structure showed no oxide formation even after extensive exposure to molecular oxygen. The usage of atomic oxygen, however, allows for oxidation of this surface and the growth of thicker oxides on both types of overlayers. At 500 °C this process is accompanied by substantial roughening of the surface.}, language = {en} } @misc{PożarowskaPleinesPrietoetal., author = {Pożarowska, Emilia and Pleines, Linus and Prieto, Mauricio J. and Tănase, Liviu C. and de Souza Caldas, Lucas and Tiwari, Aarti and Schmidt, Thomas and Falta, Jens and Morales, Carlos and Flege, Jan Ingo}, title = {The relationship between Sm alloying and structure sensitivity of ceria(111)- and (100)-oriented nanoislands on Cu(111)}, series = {Physical chemistry, chemical physics}, volume = {27}, journal = {Physical chemistry, chemical physics}, number = {29}, publisher = {Royal Society of Chemistry (RSC)}, address = {Cambridge}, issn = {1463-9076}, doi = {10.1039/D5CP01171J}, pages = {15691 -- 15703}, abstract = {We have investigated the complex dynamics of samarium deposition on ceria islands of different orientations, namely (111) and (100), grown side by side on a Cu(111) single-crystal substrate, followed by post-oxidation and annealing under ultra-high vacuum conditions. Only the (100)-oriented ceria islands undergo substantial initial reduction upon samarium deposition at 740 K via a pathway similar to the strong Ce-ceria interfacial interaction, while the (111)-oriented islands remain in the Ce4+ oxidation state. This remarkable structure sensitivity is explained by the different energies required for oxygen vacancy formation for both oxide orientations. Subsequent mild re-oxidation with O2 results in the complete recovery of the Ce4+ oxidation state in the (100)-oriented islands, indicating the complete healing of oxygen vacancies. In contrast, extended annealing at moderate temperatures likely induces persistent samarium incorporation into the cerium oxide matrix. Our results provide new insights into the complex structure-activity relationships in mixed rare-earth metal oxide systems and have promising implications for optimizing catalytic reactions over such compounds in reducing environments.}, language = {en} } @misc{AckermannPeilQuarzetal., author = {Ackermann, G. and Peil, M. and Quarz, C. and Schmidt, A. and Halaczkiewicz, M. and Thomas, A. D. and Stegm{\"u}ller, S. and Richling, E. and Manolikakes, G. and Christmann, M. and K{\"u}pper, Jan-Heiner and Schrenk, D. and Fahrer, J.}, title = {Molecular dosimetry of estragole and 1′-hydroxyestragole-induced DNA adduct formation, clastogenicity and cytotoxicity in human liver cell models}, series = {Archives of toxicology}, volume = {99}, journal = {Archives of toxicology}, number = {9}, publisher = {Springer}, address = {Berlin ; Heidelberg}, issn = {0340-5761}, doi = {10.1007/s00204-025-04084-2}, pages = {3769 -- 3785}, abstract = {The phenylpropene estragole (ES) is found in essential oils of herbs and spices, such as bitter fennel and basil. Humans are exposed to ES through the diet and phytomedicines. After its absorption, ES undergoes metabolic activation by CYP1A2 and SULT1A1 in the liver, which can give rise to DNA adducts and hepatocarcinogenesis. Until now, quantitative genotoxicity data for ES in human liver cells are scarce, correlating DNA adduct levels with critical effects such as clastogenicity. Here, we used human HepG2 and HepG2-CYP1A2 cells as well as primary human hepatocytes (PHH) to study the genotoxic, clastogenic and cytotoxic potential of ES and its crucial metabolite 1′-hydroxyestragole (1′OH-ES). In addition, primary rat hepatocytes (PRH) were used for selected endpoints. Treatment of HepG2-CYP1A2 cells with ES (0-2 mM) led to the concentration-dependent formation of E3′- N 2 -dG adducts. Apart from a moderate γH2AX induction, neither p53 accumulation nor cytotoxicity was observed. However, clastogenicity was demonstrated at ES concentrations ≥ 1 mM. Incubation of HepG2 cells with 1′OH-ES (0—35 µM) led to 10-50-fold higher E3′- N 2 -dG adduct levels compared to equimolar ES concentrations. Furthermore, 1′OH-ES caused γH2AX formation, p53 accumulation and cytotoxicity, which was confirmed in PHH. In agreement, 1′OH-ES induced clastogenicity at concentrations ≥ 25 µM. Molecular dosimetry revealed that a certain E3′- N 2 -dG adduct level is required to trigger clastogenicity and cytotoxicity. This was confirmed by Benchmark Concentration (BMC) modelling, showing that the BMC for clastogenicity is 12-17-fold higher than the respective BMC for DNA adduct formation. Our data indicate that a threshold level of DNA adducts is required, both in rat and human liver cells, to trigger markers of clastogenicity. These levels are unlikely to be reached in humans following chronic ES exposure through phytomedicines or the diet.}, language = {en} }