Ferroptosis bridges early-life oxidative stress and lifetime meat quality defects in broilers

  • Poult Sci. 2026 May 15;105(8):107133. doi: 10.1016/j.psj.2026.107133.
Xuyang Gao  1 ,  Caiwei Luo  2 ,  Bo Wang  3 ,  Jianmin Yuan  4
Affiliations
  • 1. State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China. Electronic address: [email protected].
  • 2. State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China. Electronic address: [email protected].
  • 3. State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China. Electronic address: [email protected].
  • 4. State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China. Electronic address: [email protected].
PMID: 42184739 DOI: 10.1016/j.psj.2026.107133
Abstract

This study investigated whether oxidized oil impairs broiler meat quality by triggering Ferroptosis and evaluated the synergistic protective effect of composite Antioxidants compared with individual Antioxidants. The study integrated in vivo broiler trials with in vitro cell models. First, the effects of normal oil and oxidized oil on meat quality were compared through a broiler feeding trial, and the relief effects of BHT (54 g/ton), EQ (90 g/ton), and their complexes BHT+EQ (BE; 18 and 15 g/ton) and BHT+EQ+citric acid blend (BEC; 18, 15, and 9 g/ton) were evaluated using the oxidized oil group as a positive control. Subsequently, an oxidative damage model was constructed using in ovo injection technology, and its muscle satellite cells were isolated to evaluate their potential for proliferation and differentiation, finally focusing on the Nrf2-GPX4 axis to reveal the molecular mechanism by which composite Antioxidants alleviate the meat quality deterioration caused by oxidized oil. The results found that, compared with normal oil, oxidized oil significantly impaired the meat quality of broilers, manifested as a decrease pH24h and redness (a*), while drip loss and cooking loss increased, antioxidant defense capacity was damaged, and myoglobin was unstable (P < 0.05). Antioxidant intervention can significantly alleviate the above negative effects (P < 0.05), among which the protective effect of the BEC group was the most outstanding, superior to the BE group and individual antioxidant treatments. At the cellular level, compared with normal oil, oxidized oil inhibited the abundance of Pax7 and MyHC and induced mitochondrial dysfunction (P < 0.05). The synergized BE and BEC groups effectively cleared Reactive Oxygen Species and inhibited GPX4-mediated Ferroptosis by activating the Nrf2-GPX4 signaling axis and upregulating cytoprotective genes such as NQO1 and HO-1, thereby maintaining cellular redox homeostasis. In summary, oxidized oils cause meat quality deterioration by triggering Nrf2-GPX4-mediated Ferroptosis, the BEC composite strategy confirmed in this study provides an important theoretical basis for the precise regulation of meat quality and the optimization of antioxidant programs in poultry production.

Keywords
Broiler; Ferroptosis; Meat quality; Oxidative stress; Synergistic intervention.
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