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10. Fostering healthy aging through selective nutrition: A long-term comparison of two dietary patterns and their holistic impact on mineral status in middle-aged individuals—A randomized controlled intervention trial in Germany

Author

Pellowski, Denny, Heinze, Tom, Tuchtenhagen, Max, Müller, Sandra M., Meyer, Sören, Maares, Maria, Gerbracht, Christiana, Wernicke, Charlotte, Haase, Hajo, Kipp, Anna P., Grune, Tilman, Pfeiffer, Andreas F.H., Mai, Knut, and Schwerdtle, Tanja

Published
2024
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13. Excessive copper impairs intrahepatocyte trafficking and secretion of selenoprotein P

Author

Schwarz, Maria, Meyer, Caroline E., Löser, Alina, Lossow, Kristina, Hackler, Julian, Ott, Christiane, Jäger, Susanne, Mohr, Isabelle, Eklund, Ella A., Patel, Angana A. H., Gul, Nadia, Alvarez, Samantha, Altinonder, Ilayda, Wiel, Clotilde, Maares, Maria, Haase, Hajo, Härtlova, Anetta, Grune, Tilman, Schulze, Matthias B., Schwerdtle, Tanja, Merle, Uta, Zischka, Hans, Sayin, Volkan I., Schomburg, Lutz, and Kipp, Anna P.

Published
2023
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21. Conceptual basis for the development of guidance for the use of biomarkers of effect in regulatory risk assessment of chemicals.

Author

Hernández‐Jerez, Antonio, Hougaard Bennekou, Susanne, Hoogenboom, Laurentius, Mcardle, Henry, Pieper, Christina, Schwerdtle, Tanja, Van Loveren, Hendrik, Al Harraq, Zainab, Croera, Cristina, Christodoulidou, Anna, De Sesmaisons, Agnès, Eskes, Chantra, Levorato, Sara, Valtueña Martínez, Silvia, Bompola, Georgia, and Farcal, Lucian

Subjects
TECHNICAL reports, BIOMARKERS, RISK assessment, FEASIBILITY studies, INTENTION
Abstract

This Scientific Report was carried out in the context of the self‐task mandate (M‐2023‐00097) of the EFSA's Scientific Committee on 'Guidance on the use of biomarkers of effect in regulatory risk assessment of chemicals'. In the first phase, the project on biomarkers of effect started with a feasibility study (EFSA‐Q‐2024‐00128), with the intention to look closer at definitions and descriptions of biomarkers of effect, as well as to explore several concepts related to the context of application and other scientific principles to be further considered for its development. In addition, relevant activities, initiatives and knowledge in this area were collected and analysed within a complementary mapping study. The outcome of this phase aimed to create a structured basis for future guidance, to identify challenges and to recommend a way forward for its development. The recommendations refer especially to terminologies, the scope of the guidance and several scientific and technical aspects of the selection and interpretation of biomarkers of effect that need to be addressed in future guidance. Moreover, further recommendation refers to the collaborative process to be established with other regulatory organisations that should support the harmonisation and reduce divergencies in the application of methodologies across organisations or sectors. [ABSTRACT FROM AUTHOR]

Published
2024
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35. Copper-mediated neurotoxicity and genetic vulnerability in the background of neurodegenerative diseases in C. elegans.

Author

Weishaupt, Ann-Kathrin, Ruecker, Lysann, Meiners, Torben, Schwerdtle, Tanja, Avila, Daiana Silva, Aschner, Michael, and Bornhorst, Julia

Subjects
ETIOLOGY of diseases, PARKINSON'S disease, ALZHEIMER'S disease, COPPER poisoning, IDIOPATHIC diseases, DOPAMINE receptors, DOPAMINERGIC neurons
Abstract

The mechanisms associated with neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), have yet to be fully characterized, and genetic as well as environmental factors in their disease etiology are underappreciated. Although mutations in genes such as PARKIN and LRRK2 have been linked to PD, the idiopathic component of the disease suggests a contribution of environmental risk factors, including metals, such as copper (Cu). Cu overexposure has been reported to cause oxidative stress and neurotoxicity, but its role in neurodegenerative diseases is rarely studied. Using Caenorhabditis elegans (C. elegans) as a model organism for neurotoxicity, we assessed the effects of Cu oversupply in AD and PD models. Our findings reveal that although copper treatment did not induce neurodegeneration in wild-type worms or the AD model, it significantly exacerbated neurodegeneration in the PD-associated mutants PARKIN and LRRK2. These results suggest that genetic predisposition for PD enhances the sensitivity to copper toxicity, highlighting the multifactorial nature of neurodegenerative diseases. Furthermore, our study provides insight into the mechanisms underlying Cu-induced neurotoxicity in PD models, including disruptions in dopamine levels, altered dopamine-dependent behavior and degraded dopaminergic neurons. Overall, our novel findings contribute to a better understanding of the complex interactions between genetic susceptibility, environmental factors, and neurodegenerative disease pathogenesis, emphasizing the importance of a tightly regulated Cu homeostasis in the etiology of PD. Copper oversupply exacerbated neurodegeneration in Caenorhabditis elegans models of Parkinson's disease, highlighting the genetic susceptibility and emphasizing the crucial role of tightly regulated copper homeostasis in Parkinson's disease pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Update of the risk assessment of brominated phenols and their derivatives in food.

Author

Knutsen, Helle Katrine, Åkesson, Agneta, Bampidis, Vasileios, Bignami, Margherita, Bodin, Laurent, Chipman, James Kevin, Degen, Gisela, Hernández‐Jerez, Antonio, Hofer, Tim, Landi, Stefano, Leblanc, Jean‐Charles, Machera, Kyriaki, Ntzani, Evangelia, Rychen, Guido, Sand, Salomon, Schwerdtle, Tanja, Vejdovszky, Katharina, Viviani, Barbara, Benford, Diane, and Hart, Andy

Subjects
PHENOL derivatives, RISK assessment, DATABASES, BODY weight, BROMOPHENOLS
Abstract

The European Commission asked EFSA to update its 2012 risk assessment on brominated phenols and their derivatives in food, focusing on five bromophenols and one derivative: 2,4,6‐tribromophenol (2,4,6‐TBP), 2,4‐dibromophenol (2,4‐DBP), 4‐bromophenol (4‐BP), 2,6‐dibromophenol (2,6‐DBP), tetrabrominated bisphenol S (TBBPS), tetrabromobisphenol S bismethyl ether (TBBPS‐BME). Based on the overall evidence, the CONTAM Panel considered in vivo genotoxicity of 2,4,6‐TBP to be unlikely. Effects in liver and kidney were considered as the critical effects of 2,4,6‐tribromophenol (2,4,6‐TBP) in studies in rats. A BMDL10 of 353 mg/kg body weight (bw) per day for kidney papillary necrosis in male rats was identified and was selected as the reference point for the risk characterisation. The derivation of a health‐based guidance value was not considered appropriate due to major limitations in the toxicological database. Instead, the margin of exposure (MOE) approach was applied to assess possible health concerns. Around 78,200 analytical results for 2,4,6‐TBP in food were used to estimate dietary exposure for the European population. Considering the resulting MOE values, all far above an MOE of 6000 that does not raise a health concern, and accounting for the uncertainties affecting the exposure and hazard assessments, the CONTAM Panel concluded with at least 95% probability that the current dietary exposure to 2,4,6‐TBP does not raise a health concern. Due to lack of occurrence data, no risk assessment could be performed for breastfed or formula‐fed infants. No risk characterisation could be performed for any of the other brominated phenols and derivatives included in the assessment, due to lack of data both on the toxicity and occurrence. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Genotoxicity of beauvericin.

Author

Knutsen, Helle Katrine, Åkesson, Agneta, Bampidis, Vasileios, Bodin, Laurent, Chipman, James Kevin, Degen, Gisela, Hernández‐Jerez, Antonio, Hofer, Tim, Hogstrand, Christer, Landi, Stefano, Leblanc, Jean‐Charles, Machera, Kyriaki, Ntzani, Evangelia, Rychen, Guido, Sand, Salomon, Schwerdtle, Tanja, Vejdovszky, Katharina, Viviani, Barbara, Corsini, Emanuela, and Le Hégarat, Ludovic

Subjects
STRUCTURE-activity relationships, DNA repair, CHROMOSOME abnormalities, BEAUVERICIN, GENE expression
Abstract

The European Commission (EC) asked EFSA to assess the genotoxicity of beauvericin (BEA). Relevant information, including that which has become available since the 2014 Scientific Opinion on the risks to human and animal health related to the presence of BEA and enniatins in food and feed, was reviewed. In the previous Opinion the Panel concluded that in vitro genotoxicity data were equivocal and there were no in vivo genotoxicity data available. New in vitro studies in mammalian cell lines provided no convincing evidence for induction of chromosomal damage by BEA as measured by micronucleus and chromosome aberration tests or an increase of DNA strand breaks as assessed by the Comet assay. In these studies, no concentration‐dependent effects or potential for interference from associated cytotoxicity were observed. In addition, DNA double‐strand breaks as measured by γ‐H2AX analysis were only observed following exposure to highly cytotoxic BEA concentrations. In vivo studies (Comet and Pig‐a assays, micronucleus test) with BEA were negative. In vitro gene expression studies showed no indication of a DNA damage response and (quantitative) structure activity relationship analysis was also not indicative of genotoxic potential. Some effects of BEA might play an indirect role in the formation of DNA strand breaks. These include increased reactive oxygen species, induction of cell cycle arrest and apoptosis, associated with interference in mitochondrial function and cell signalling. There was no compelling evidence of inflammatory and immunosuppressive effects. Taken together, the available data indicate that BEA is devoid of genotoxic potential. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Impact of peripheral thyroid hormone balance on liver fat: insights from the NutriAct trial.

Author

Sommer-Ballarini, Miriam, Nguyen, Thu-Huong, Pletsch-Borba, Laura, Wernicke, Charlotte, Tacke, Frank, Schwerdtle, Tanja, Pellowski, Denny, Machann, Jürgen, Spranger, Joachim, Wirth, Eva Katrin, and Mai, Knut

Subjects
NUCLEAR magnetic resonance spectroscopy, UNSATURATED fatty acids, FATTY liver, REDUCING diets, LIPID metabolism
Abstract

Objective Hypothyroidism has been proposed as a potential contributor to steatotic liver disease (SLD), but existing data shows conflicting results in euthyroid subjects. Therefore, we investigated the association between thyroid function and intrahepatic lipids (IHLs) during a 36-month randomized controlled trial evaluating a diet known to reduce liver fat. Design 502 eligible subjects (aged 50–80 years, ≥1 risk factor for unhealthy aging) were randomly assigned to either follow a diet rich in unsaturated fatty acids, plant protein, and fiber (intervention group, IG), or dietary recommendations of the German Nutrition Society (control group, CG). Methods Serum levels of thyroid hormones (THs) as well as IHLs, defined via magnetic resonance spectroscopy, were measured within an euthyroid subgroup without significant alcohol consumption at baseline (n = 332) and after 12 months (n = 243). A ratio of T3/T4 was used to assess whole-body deiodinase activity. Estimates of glucose and lipid metabolism were analyzed. Results Only fT3 and T3/T4 ratios showed a significant positive correlation with IHL at baseline. We observed a significant decline in fT3, T3, fT3/fT4 ratio, and T3/T4 ratio in CG and IG after 12 months without significant differences between groups. TSH, fT4, and T4 remained stable. A larger improvement of IHL during dietary intervention was seen in those subjects with a lower decline in T3 concentrations. Conclusions Altered TH balance indicates a possible compensatory upregulation of whole-body TH activity in subjects with increased liver fat. This might be also relevant during the improvement of hepatic steatosis. [ABSTRACT FROM AUTHOR]

Published
2024
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