L-carnosine alleviates wooden breast myopathy in broilers fed oxidized soybean oil: Focus on antioxidant defense, calcium homeostasis, and satellite cell function.

Feeding oxidized soybean oil (OSO) can disrupt the redox homeostasis in broilers and increase the incidence and severity of wooden breast (WB) myopathy. The antioxidant activity of L-carnosine (LC) has been demonstrated to help alleviate oxidative stress generated during metabolic processes. Therefore, the effects of dietary LC supplementation on WB myopathy were investigated in this study. One hundred and twenty-six 21-d-old white-feathered broilers (1.017 ± 0.039 kg) were randomly allocated into three groups (7 replicates per group with 6 broilers per replicate): fresh soybean oil group (CON), OSO group (OSO), and OSO + 800 mg/kg LC (OSO + LC), for a 21-d trial. Compared with the CON group, broilers in the OSO group showed an increased feed-to-gain ratio, elevated reactive oxygen species (ROS) and malondialdehyde (MDA) contents, and decreased LC content in the pectoralis major (PM) muscle (P < 0.05). Concurrently, disrupted muscle calcium homeostasis was observed in the OSO group, characterized by significant upregulation of calcium-regulating proteins such as MCU, RYR, and NCX, together with downregulation of SERCA in the PM muscle (P < 0.05). Upregulation of MYOD and PAX7 along with downregulation of MYF6 was observed in the OSO group compared to the CON group (P < 0.05). Furthermore, the OSO group showed a 33.34% higher incidence of WB and increased muscle collagen deposition than the CON group (P < 0.05). Compared with the OSO group, broilers in the OSO + LC group exhibited reduced levels of oxidative stress markers (ROS, MDA, and protein carbonyls) and increased levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), total antioxidant capacity (T-AOC) and LC in the PM muscle (P < 0.05). Muscle calcium homeostasis was rebalanced in the OSO + LC group through downregulation of IP3R, MCU, NCX, RYR, and PMCA, combined with upregulation of SERCA (P < 0.05). Moreover, the numbers of MYOD+ and PAX7+ cells in PM muscle of the OSO + LC group were lower than those of the OSO group (P < 0.05). Collagen deposition in the OSO + LC group was significantly reduced (P < 0.001) along with a decreasing trend in WB incidence compared to the OSO group (P = 0.043). The results indicate that OSO induces WB myopathy through oxidative stress, while LC effectively mitigates its adverse effects.