Mitochondrial dysfunction and calcium dyshomeostasis in the pectoralis major muscle of broiler chickens with wooden breast myopathy
文献类型： 外文期刊
作者： Zhang, Xinrui 1 ; Xing, Tong 1 ; Li, Jiaolong 2 ; Zhang, Lin 1 ; Gao, Feng 1 ;
作者机构： 1.Nanjing Agr Univ, Jiangsu Collaborat Innovat Ctr Meat Prod & Proc Qu, Key Lab Anim Origin Food Prod & Safety Guarantee J, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China
2.Jiangsu Acad Agr Sci, Inst Agriprod Proc, Nanjing 210014, Peoples R China
关键词： woodenbreast; broilerchicken; mitochondrialfunction; mitochondrialredoxstatus; Ca2+ homeostasis
期刊名称：POULTRY SCIENCE （ 影响因子：4.4； 五年影响因子：4.4 ）
ISSN： 0032-5791
年卷期： 2023 年 102 卷 9 期
页码：
收录情况： SCI
摘要： 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 poten-tial mechanisms are not fully understood. This study aimed to explore the underlying mechanism of the dam -age of WB-affected PM muscle caused by changes in mitochondrial function, mitochondrial redox status and Ca2+ 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 Ca2+ channels led to substantial Ca2+ loss in SR and cyto-plasmic Ca2+ overload, as well as Ca2+ accumulation in mitochondria, resulting in Ca2+ dyshomeostasis in PM muscle of broiler chickens with WB myopathy. Com-bined, these findings indicate that WB myopathy is related to mitochondrial dysfunction, mitochondrial redox status imbalance and Ca2+ dyshomeostasis, leading to WB-affected PM muscle damage.
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