Ferroptosis is an iron-dependent regulated cell death characterized by lipid peroxidation. In the skeletal muscle of mammals, where oxidative stress plays an important role in lipid peroxidation, ferroptosis is involved in various diseases and aging. However, the role of ferroptosis in avian skeletal muscle remains underexplored. This study investigated the gene expression of glutathione peroxidase 4 (GPX4) and other ferroptosis-related genes, along with oxidative stress markers in chicken skeletal muscles, focusing on the breast (pectoralis major) and thigh (iliotibialis lateralis) muscles. Gene expression was analyzed using quantitative reverse transcription polymerase chain reaction. Lipid peroxidation and oxidative stress were evaluated by measuring malondialdehyde (MDA), a lipid peroxidation byproduct, and by evaluating the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG). Our results showed that GPX4 gene expression was significantly higher in the thigh muscle compared to the breast muscle. Ferroptosis suppressor protein 1 (FSP1) expression was also higher in the thigh muscle, while ferritin heavy chain 1 (FTH1) expression was lower in the thigh muscle than in the breast muscle. In contrast, lipid peroxidation, indicated by MDA levels, was higher in the breast muscle, correlating with a lower GSH/GSSG ratio, indicating that the breast muscle is more susceptible to ferroptosis than the thigh muscle. Additionally, the expression of FSP1 and FTH1 showed significant correlations with oxidative stress markers, highlighting their roles in regulating ferroptosis in avian skeletal muscle. This study provides insights into the molecular mechanisms of ferroptosis in avian skeletal muscle, suggesting that regulatory processes may vary between muscle types.
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