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. 2026 Feb 7;100(5):1903–1926. doi: 10.1007/s00204-026-04303-4

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© The Author(s) 2026

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 5 — Metabolomic alterations induced by PTU and PCN in liver, brain, and thyroid tissues at different developmental stages. a Upset plots representing the distribution of the top 50 discriminant metabolites in liver, brain, and thyroid tissues of rat at GD21 and PND21 following in utero exposure to PTU or PCN. Each bar represents the number of unique or shared altered metabolites across the different treatment-timepoint combinations. b Heatmap of the most relevant brain metabolites identified by PLS-DA, representing their abundance profiles across treatments (PCN or PTU) and timepoints (GD21 and PND21). Metabolites are hierarchically clustered, and color scale indicates standardized abundance (Z-score)