Lipid peroxidation driven by polyunsaturated fatty acid (PUFA) oxidation compromises feed quality and animal health. Single antioxidants (e.g., ethoxyquin (EQ), butylated hydroxytoluene (BHT)) face limitations including dose-dependent toxicity, bioaccumulation risks, and inadequate protection against multistage oxidation. Composite systems leveraging complementary mechanisms offer a promising alternative. This study evaluated synergistic efficacy of rationally formulated composite antioxidants (combining synthetic radical scavengers and metal chelators) versus single-component systems in enhancing lipid oxidative stability in high-fat animal feed. The basal diet containing oxidized oil served as the control group (CON). Seven groups were supplemented with the basal diet as follows: Treatment A, 36 g/ton Butylated Hydroxytoluene (BHT); Treatment B, 60 g/ton Ethoxyquin (EQ); Treatment C, 132 g/ton EQ; Treatment D, 10 g/ton EQ + 12 g/ton BHT; Treatment E, 10 g/ton EQ + 12 g/ton BHT + 6 g/ton Citric acid (CA); Treatment F, 20 g/ton EQ + 6 g/ton BHT + 6 g/ton CA; and treatment G, 2 g/ton EQ + 25 g/ton BHT + 6 g/ton CA. Oxidative stability was assessed over a 10-week period under natural storage (T0-T10) and acute thermal stress (120 °C drying for 2 h followed by ambient storage; HT0 to HT10). Oxidative stability was assessed via: antioxidant capacity (DPPH (2,2-Diphenyl-1-picrylhydrazyl)/ABTS (2,2′-Azinobis (3-ethylbenzothiazoline-6-sulfonic acid) scavenging, total antioxidant capacity), physical indices: Color (L*, a*, b*), and chemical oxidation markers: conjugated dienes (CD), peroxide value (PV), p-anisidine value (p-AV), malondialdehyde (MDA), acid value (AV), total oxidation (TOTOX). Superior synergistic performance of the ternary blend (Treatment E) was demonstrated versus singles (A/B/C). Retention of radical scavenging capacity was significantly enhanced, with greater stability observed under accelerated storage. Primary oxidation (PV) and secondary oxidation (MDA, p-AV) were most effectively suppressed by Treatment E. Superior color stability (minimal L* change) was maintained under thermal stress. The lowest TOTOX values were achieved across all conditions by Treatment E. Stage-specific vulnerabilities were shown by single antioxidants (BHT volatilization; pro-oxidative effects of EQ at high doses). Comprehensive, temperature-resilient protection was delivered collectively by the synergistic EQ+BHT+CA system (Treatment E) via combined radical quenching and metal chelation. The inherent limitations of individual antioxidants were effectively overcome by the optimized composite, enabling reduced total dosage while substantially extending the lipid oxidative stability period.

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 pH_24h 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.

(−)-Epigallocatechin 3-gallate (EGCG) is a potent natural antioxidant, but its strong bitterness and poor palatability limit its application in animal production. This study aimed to evaluate the protective effects and underlying mechanisms of chemically synthesized EGCG derivatives against oxidative stress using a diquat-induced mouse model. A total of 36 male ICR mice were randomly assigned into six groups (n = 6): Control (T0), Diquat (T1), EGCG + Diquat (T2), Epigallocatechin octanoate (EGCO) + Diquat (T3), Epigallocatechin p-chloromethylbenzoate (EGCP) + Diquat (T4), and Epigallocatechin ibuprofen ester (EGCI) + Diquat (T5). Oxidative stress was induced by intraperitoneal injection of diquat at day 27 of the experiment, while EGCG or its derivatives were administered via dietary supplementation. At day 28, the mice were weighed, killed, and the tissues were sampled. Diquat challenge significantly impaired growth, increased serum injury markers (ALT, AST, DAO, and D-LA) (p < 0.05), suppressed hepatic and jejunal antioxidant enzymes (GPx, SOD, and TAOC) while elevating MDA (p < 0.05), damaged jejunal morphology (villus atrophy) (p < 0.05), and downregulated tight junction proteins (ZO-1 and Occludin) (p < 0.05). Chemically synthesized EGCG derivatives, especially EGCI, effectively alleviated diquat-induced growth impairment and hepatic and intestinal oxidative damage by improving intestinal barrier function and enhancing systemic antioxidant capacity, possibly in part through activation of the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway. Compared with EGCG, EGCI exhibited reduced bitterness and improved palatability, which favored normal feed intake. These findings provide strong theoretical support for the future application of EGCG derivatives, especially EGCI, as functional antioxidant additives in broiler production.