@article{EbertZiemannWandtetal.2020,
  author    = {Ebert, Franziska and Ziemann, Vanessa and Wandt, Viktoria Klara Veronika and Witt, Barbara and M{\"u}ller, Sandra Marie and Guttenberger, Nikolaus and Bankoglu, Ezgi Eyluel and Stopper, Helga and Raber, Georg and Francesconi, Kevin A. and Schwerdtle, Tanja},
  title     = {Cellular toxicological characterization of a thioxolated arsenic-containing hydrocarbon},
  series = {Journal of trace elements in medicine and biology},
  volume    = {61},
  journal   = {Journal of trace elements in medicine and biology},
  publisher = {Elsevier},
  address   = {M{\"u}nchen},
  doi       = {10.1016/j.jtemb.2020.126563},
  year      = {2020},
  abstract  = {Arsenolipids, especially arsenic-containing hydrocarbons (AsHC), are an emerging class of seafood originating contaminants. Here we toxicologically characterize a recently identified oxo-AsHC 332 metabolite, thioxo-AsHC 348 in cultured human liver (HepG2) cells. Compared to results of previous studies of the parent compound oxo-AsHC 332, thioxo-AsHC 348 substantially affected cell viability in the same concentration range but exerted about 10-fold lower cellular bioavailability. Similar to oxo-AsHC 332, thioxo-AsHC 348 did not substantially induce oxidative stress nor DNA damage. Moreover, in contrast to oxo-AsHC 332 mitochondria seem not to be a primary subcellular toxicity target for thioxo-AsHC 348. This study indicates that thioxo-AsHC 348 is at least as toxic as its parent compound oxo-AsHC 332 but very likely acts via a different mode of toxic action, which still needs to be identified.},
  language  = {en}
}
@article{FinkeWandtEbertetal.2020,
  author    = {Finke, Hannah and Wandt, Viktoria Klara Veronika and Ebert, Franziska and Guttenberger, Nikolaus and Glabonjat, Ronald A. and Stiboller, Michael and Francesconi, Kevin A. and Raber, Georg and Schwerdtle, Tanja},
  title     = {Toxicological assessment of arsenic-containing phosphatidylcholines in HepG2 cells},
  volume    = {12},
  number    = {7},
  publisher = {Oxford University},
  address   = {Cambridge},
  doi       = {10.1039/d0mt00073f},
  pages     = {1159 -- 1170},
  year      = {2020},
  abstract  = {Arsenolipids include a wide range of organic arsenic species that occur naturally in seafood and thereby contribute to human arsenic exposure. Recently arsenic-containing phosphatidylcholines (AsPCs) were identified in caviar, fish, and algae. In this first toxicological assessment of AsPCs, we investigated the stability of both the oxo- and thioxo-form of an AsPC under experimental conditions, and analyzed cell viability, indicators of genotoxicity and biotransformation in human liver cancer cells (HepG2). Precise toxicity data could not be obtained owing to the low solubility in the cell culture medium of the thioxo-form, and the ease of hydrolysis of the oxo-form, and to a lesser degree the thioxo-form. Hydrolysis resulted amongst others in the respective constituent arsenic-containing fatty acid (AsFA). Incubation of the cells with oxo-AsPC resulted in a toxicity similar to that determined for the hydrolysis product oxo-AsFA alone, and there were no indices for genotoxicity. Furthermore, the oxo-AsPC was readily taken up by the cells resulting in high cellular arsenic concentrations (50 μM incubation: 1112 ± 146 μM As cellular), whereas the thioxo-AsPC was substantially less bioavailable (50 μM incubation: 293 ± 115 μM As cellular). Speciation analysis revealed biotransformation of the AsPCs to a series of AsFAs in the culture medium, and, in the case of the oxo-AsPC, to as yet unidentified arsenic species in cell pellets. The results reveal the difficulty of toxicity studies of AsPCs in vitro, indicate that their toxicity might be largely governed by their arsenic fatty acid content and suggest a multifaceted human metabolism of food derived complex arsenolipids.},
  language  = {en}
}
@article{FinkeWinkelbeinerLossowetal.2020,
  author    = {Finke, Hannah and Winkelbeiner, Nicola Lisa and Lossow, Kristina and Hertel, Barbara and Wandt, Viktoria Klara Veronika and Schwarz, Maria and Pohl, Gabriele and Kopp, Johannes Florian and Ebert, Franziska and Kipp, Anna Patricia and Schwerdtle, Tanja},
  title     = {Effects of a Cumulative, Suboptimal Supply of Multiple Trace Elements in Mice},
  series = {Molecular nutrition \& food research},
  volume    = {64},
  journal   = {Molecular nutrition \& food research},
  number    = {16},
  publisher = {Wiley-VCH},
  address   = {Weinheim},
  issn      = {1613-4125},
  doi       = {10.1002/mnfr.202000325},
  year      = {2020},
  abstract  = {Scope: Trace element (TE) deficiencies often occur accumulated, as nutritional intake is inadequate for several TEs, concurrently. Therefore, the impact of a suboptimal supply of iron, zinc, copper, iodine, and selenium on the TE status, health parameters, epigenetics, and genomic stability in mice are studied. Methods and results: Male mice receive reduced or adequate amounts of TEs for 9 weeks. The TE status is analyzed mass-spectrometrically in serum and different tissues. Furthermore, gene and protein expression of TE biomarkers are assessed with focus on liver. Iron concentrations are most sensitive toward a reduced supply indicated by increased serum transferrin levels and altered hepatic expression of iron-related genes. Reduced TE supply results in smaller weight gain but higher spleen and heart weights. Additionally, inflammatory mediators in serum and liver are increased together with hepatic genomic instability. However, global DNA (hydroxy)methylation is unaffected by the TE modulation. Conclusion: Despite homeostatic regulation of most TEs in response to a low intake, this condition still has substantial effects on health parameters. It appears that the liver and immune system react particularly sensitive toward changes in TE intake. The reduced Fe status might be the primary driver for the observed effects.},
  language  = {en}
}