College of Animal Science and Technology, Key Laboratory of Animal Origin Food Production and Safety Guarantee of Jiangsu Province, Jiangsu Collaborative Innovation Center of Meat Production and Processing, Quality and Safety Control, Nanjing Agricultural University, Nanjing 210095, PR China.
Institute of Agri-Products Processing, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, PR China.
Poult Sci. 2023 Sep;102(9):102872. doi: 10.1016/j.psj.2023.102872. Epub 2023 Jun 14.
The incidence of wooden breast (WB) meat of commercial broiler chicken has been increasing in recent years. Histological examination found that the occurrence of WB myopathy was accompanied by the pectoralis major (PM) muscle damage. So far, the potential mechanisms are not fully understood. This study aimed to explore the underlying mechanism of the damage of WB-affected PM muscle caused by changes in mitochondrial function, mitochondrial redox status and Ca homeostasis. A total of 80 market-age Arbor Acres male broiler chickens were sampled and categorized into control (CON) and WB groups based on the evaluation of myopathic lesions. PM muscle samples were collected (n = 8 in each group) for histopathological evaluation and biochemical analyses. Ultrastructural examination and histopathological changes suggested the occurrence of PM muscle damage in broiler chickens with WB myopathy. The WB group showed an increased level of reactive oxygen species and enhanced antioxidant capacities in mitochondria of PM muscle. These changes were related to impaired mitochondria morphology and mitochondrial dysfunction. In addition, abnormal expressions of Ca channels led to substantial Ca loss in SR and cytoplasmic Ca overload, as well as Ca accumulation in mitochondria, resulting in Ca dyshomeostasis in PM muscle of broiler chickens with WB myopathy. Combined, these findings indicate that WB myopathy is related to mitochondrial dysfunction, mitochondrial redox status imbalance and Ca dyshomeostasis, leading to WB-affected PM muscle damage.
近年来，商业肉鸡的木质鸡胸（WB）肉的发病率一直在增加。组织学检查发现，WB 肌病的发生伴随着胸大肌（PM）肌肉损伤。迄今为止，其潜在机制尚未完全阐明。本研究旨在探讨线粒体功能、线粒体氧化还原状态和 Ca 稳态改变导致 WB 受累 PM 肌肉损伤的潜在机制。共采集了 80 只市场年龄的 Arbor Acres 雄性肉鸡，根据肌病病变的评估，将其分为对照组（CON）和 WB 组。采集 PM 肌肉样本（每组 8 只）进行组织病理学评估和生化分析。超微结构检查和组织病理学变化表明，患有 WB 肌病的肉鸡 PM 肌肉损伤的发生。WB 组 PM 肌肉中线粒体的活性氧水平升高，抗氧化能力增强。这些变化与线粒体形态受损和线粒体功能障碍有关。此外，Ca 通道的异常表达导致 SR 和细胞质中大量 Ca 丢失以及细胞质 Ca 超载，以及线粒体中 Ca 积累，导致 WB 肌病肉鸡 PM 肌肉中的 Ca 稳态失衡。综上所述，这些发现表明，WB 肌病与线粒体功能障碍、线粒体氧化还原状态失衡和 Ca 稳态失衡有关，导致 WB 受累 PM 肌肉损伤。
