文献类型： 外文期刊

第一作者： Liao, Hongju

作者： Liao, Hongju;Zhang, Lin;Li, Jiaolong;Xing, Tong;Gao, Feng;Li, Jiaolong

作者机构：

关键词： acute stress; broiler chicken; meat quality; mitochondrial function; redox status

期刊名称：JOURNAL OF ANIMAL SCIENCE （ 影响因子：3.338； 五年影响因子：3.243 ）

ISSN： 0021-8812

年卷期： 2022 年 100 卷 9 期

页码：

收录情况： SCI

摘要： Lay Summary Preslaughter acute stress can cause physiological and metabolic disorders of broilers and lead to deterioration of meat quality and high incidence of pale, soft, and exudative (PSE)-like meat, which block the development of broiler industry. Acute stress-induced imbalance of redox status and insufficient energy supply are important reasons for meat quality reduction. Mitochondria provide the overall cellular energy production through oxidative phosphorylation and play a key role in maintaining energy homeostasis. Investigating the effects of acute stress on mitochondrial function and exploring the possible mechanisms involved in mitochondrial function regulation can promote an understanding of how acute stress affects broiler meat quality. Our results indicate that pre-slaughter transport under high environmental temperature reduces energy status and induces oxidative stress in pectoralis major muscle of broilers, which contribute to the deterioration of meat quality and the increased occurrence of PSE-like meat. The oxidative damage of mitochondria and the dysregulation of mitochondrial function are responsible for the energy deficiency and redox imbalance. Although broilers improve the antioxidant capacity and enhance the biosynthesis as well as the decoupling of respiratory chain for maintaining mitochondrial function in response to acute stress, these adaptive responses are insufficient to restore mitochondrial homeostasis and redox status. 1. Acute stress causes redox imbalance and mitochondrial dysfunction in broiler muscle. 2. This study provides new aspects for understanding how acute stress affects broiler meat quality. This study investigated the effects of acute stress on breast meat quality, redox status, and mitochondrial function in pectoralis major (PM) muscle of broilers. A total of 168 broiler chickens (42-d-old, Ross 308) were randomly divided into control (CON) and preslaughter transport (T) treatments. A broiler was an experimental unit. Each treatment consisted of 84 broilers, and they were put in 12 crates with 7 broilers each. Broilers in the T group were transported according to a designed protocol, and the CON broilers were kept in crates under normal living conditions before slaughtering. Based on the meat quality traits assessed at postmortem 24 h, all PM muscles of the transported broilers were further classified into normal (T-NOR) and pale, soft, and exudative (PSE)-like (T-PSE) groups for the determination of redox status in PM muscle and isolated mitochondria, energy metabolites, mitochondrial electron transport chain complexes activities, as well as mitochondrial function-modulating genes expression. Compared with CON, the extent of lipid peroxidation as well as protein oxidation were significantly increased in both PM muscles and mitochondria in T-PSE (P < 0.05), whereas not in T-NOR. Higher activities of glutathione peroxidase, total superoxide dismutase, and Cu-Zn superoxide dismutase were observed in PM muscle of T-NOR broilers when compared with CON (P < 0.05). Preslaughter transport increased the generation of reactive oxygen species, as well as enhanced antioxidant capacity in PM mitochondria of broilers (P < 0.05). Compared with CON, the ATP content, activities of complexes I and III, as well as relative mitochondrial membrane potential and swelling were significantly decreased in T-PSE (P < 0.05), whereas no significant changes in either ATP content or complex I activity were observed in T-NOR. Preslaughter transport enhanced the mRNA expression of regulators involved in the glutathione system, thioredoxin 2 system, and mitochondrial biosynthesis in PM muscle of broilers (P < 0.05). Moreover, we noticed a more evident enhancement effect in T-NOR than in T-PSE (P < 0.05). Overall, this work indicates that acute stress-induced redox imbalance and mitochondrial dysfunction have significant implications for the development of PSE-like meat.

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