Resveratrol Pretreatment and Decabromodiphenyl Ethane-Associated Hepatorenal Changes in a High-Dose Female Mouse Model: Redox Changes and Ferroptosis-Associated Markers.

Authors

Yutong Ji, Chengzhi Liu, Xianhua Wu, Mingxian Shi, Tingjun Hu, Jiakang He, Yingyi Wei, Lei Wang, Meiling Yu

Published in

Food science & nutrition. Volume 14. Issue 10. Pages e72495. Epub Oct 16, 2026.

Abstract

Decabromodiphenyl ethane (DBDPE) is an emerging brominated flame retardant that has been detected in animal-derived foods. This exploratory experiment used a high-dose toxicological challenge rather than a dietary-exposure scenario. This study evaluated whether resveratrol (Res) pretreatment was associated with differences in selected liver- and kidney-related endpoints in a high-dose DBDPE mouse model. A total of 54 five-week-old specific pathogen-free female Kunming mice were acclimated for 7 days and allocated into six groups (n = 9) by weight-ranked allocation. Res (25, 50, or 100 mg/kg body weight/day; 100 mg/kg in the Res-alone group) or vehicle was administered by oral gavage 2 h before DBDPE (500 mg/kg body weight/day) or corn oil, also by gavage, for 28 consecutive days. DBDPE exposure was associated with serum biochemical alterations, descriptive liver and kidney histological changes, redox imbalance, higher iron-assay values, mitochondrial ultrastructural abnormalities, and changes in ferroptosis-associated markers. The liver index was 5.06% ± 0.20% in the Control group, 5.89% ± 0.60% in the DBDPE group and 5.17% ± 0.41% in the 100 mg/kg Res pretreatment group; the corresponding kidney indices were 1.02% ± 0.10%, 1.16% ± 0.07% and 1.06% ± 0.03%. Res pretreatment was accompanied by lower values for several DBDPE-associated endpoints, by changes in Pik3r1, Nfe2l2 and selected antioxidant-related transcripts, and by tissue-dependent changes in ferroptosis-associated markers. These findings provide in vivo associative evidence under the specified experimental conditions and support further evaluation of Res in DBDPE toxicology models; they do not establish ferroptotic cell death, PI3K/Nrf2 pathway activation, or relevance to typical human dietary exposure.

PMID:
42892944
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.

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