4.6 Article

Hepatic Oxidative Stress, Apoptosis, and Inflammation in Broiler Chickens With Wooden Breast Myopathy

Journal

FRONTIERS IN PHYSIOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2021.659777

Keywords

wooden breast; broiler chicken; liver; oxidative stress; apoptosis; inflammation

Categories

Funding

  1. China Postdoctoral Science Foundation [2018M640492, 2019T120432]
  2. Jiangsu Postdoctoral Science Foundation [2019K013]
  3. Natural Science Foundation of Jiangsu Province in China [BK20190516]
  4. National Natural Science Foundation of China [31872374, 32072780]
  5. National Key Research and Development Program of China [2018YFD0500405]
  6. Earmarked Fund for Jiangsu Agricultural Industry Technology System [JATS[2020]407]

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Wooden breast syndrome in broiler chickens not only affects the pectoralis major muscle but also leads to liver injury, as evidenced by higher plasma enzymes and histopathological changes in the liver. This myopathy induces oxidative stress, mitochondrial dysfunction, and hepatic apoptosis, along with inflammatory responses in the liver. Additional assessment is needed to understand the systemic physiological disparities and metabolic changes associated with wooden breast myopathy.
Wooden breast (WB) syndrome has emerged as a global myopathy in modern commercial broiler chickens, mainly affecting the pectoralis major muscle. Recent evidence suggests that WB myopathy is a systemic disease, which might be accompanied by other physiological disparities and metabolic changes. This study was conducted to systemically investigate the potential physiological changes in liver tissues as well as the possible mechanisms involved to enhance the understanding of the etiology. A total of 93 market-age Arbor Acres male broiler chickens were sampled and categorized into control (CON) and WB groups based on the evaluation of myopathic lesions. Liver samples were collected (n = 10 in each group) for histopathological evaluation and biochemical analyses. Results indicated that WB birds exhibited significantly higher plasma aspartate amino transferase, alkaline phosphatase, and gamma glutamyl transpeptidase activities. Histopathological changes in hydropic/fatty degeneration, inflammatory cell infiltration, intrahepatic hemorrhages, elevated myeloperoxidase activity, and overproduction of nitric oxide were observed in WB liver compared with CON, suggesting the occurrence of liver injury in birds affected by WB myopathy. The WB group showed increased levels of reactive oxygen species, oxidative products, as well as enhanced antioxidant capacities in the liver. These changes were associated with impaired mitochondria morphology and mitochondrial dysfunction. WB myopathy also induced mitochondria-mediated hepatic apoptosis by upregulating levels of caspases 3 and 9, altering the expressions of apoptotic B-cell lymphoma-2 family regulators, as well as increasing the release of cytochrome c. The activation of nuclear factor kappa-light-chain-enhancer of activated B cell signaling enhanced the mRNA expression of downstream inflammatory mediators, contributing to the production of inflammatory cytokines in WB liver. Combined, these findings suggest that hepatic disorders may be conjoined with WB myopathy in broiler chickens and indicating systemic physiological disparities, and other metabolic changes accompanying this myopathy need further assessment.

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