Hasegawa Yasuhiro, Hosotani Marina, Saito Miyu, Nagasawa Tatsuki, Mori Yusuke, Kawasaki Takeshi, Yamada Michi, Maeda Naoyuki, Watanabe Takafumi, Iwasaki Tomohito
Department of Food Science and Human Wellness, Rakuno Gakuen University, Ebetsu, Hokkaido, Japan.
Department of Veterinary Science, Rakuno Gakuen University, Ebetsu, Hokkaido, Japan.
Comp Biochem Physiol A Mol Integr Physiol. 2022 Nov;273:111296. doi: 10.1016/j.cbpa.2022.111296. Epub 2022 Aug 13.
The growth rate of broiler chickens has increased by 400% over the past 50 years, and breast yields continue to increase. This has led to an increase in thoracic muscle abnormalities in broilers, with wooden breast becoming a major issue worldwide. The etiology and the mechanism underlying the etiology of wooden breasts have not yet been elucidated; however, it occurs due to oxidative stress. Reactive oxygen species, which cause oxidative stress, are mainly produced in mitochondria. Thus, in this study, we investigated the relationship between the severity of wooden breast in broilers and the characteristics of mitochondria as the source of reactive oxygen species. Sampling of the pectoralis major muscle at the ventral cranial position was conducted in 50-day-old broilers. The severity of wooden breast was classified into three groups based on the muscle fiber roundness and wing-wing contact test, with highest severity in severe wooden breast and lowest severity in normal breast. Nicotinamide adenine dinucleotide tetrazolium reductase staining revealed an increase in darkly stained muscle fibers, indicating high severity of wooden breast. The mitochondria were swollen in severe wooden breast cases, with highest swelling in severe wooden breast and lowest swelling in normal breast. The expression levels of the mitochondrial antioxidant enzyme genes superoxide dismutase 1 and superoxide dismutase 2 were significantly lower in wooden breast-severe tissue than in normal tissue. These results suggest that when the levels of reactive oxygen species in muscle fibers, which should be constant, are increased, mitochondrial homeostasis is not maintained and the damage levels increase in various membranes of the cell, leading to the disruption of normal physiological functions.
在过去50年里，肉鸡的生长速度提高了400%，胸肌产量持续增加。这导致肉鸡胸肌异常增多，木胸已成为全球范围内的一个主要问题。木胸的病因及其潜在机制尚未阐明；然而，它是由氧化应激引起的。导致氧化应激的活性氧主要在线粒体中产生。因此，在本研究中，我们调查了肉鸡木胸严重程度与作为活性氧来源的线粒体特征之间的关系。在50日龄肉鸡的腹侧颅部位置采集胸大肌样本。根据肌纤维圆度和翅翅接触试验，将木胸严重程度分为三组，木胸严重组严重程度最高，正常胸组严重程度最低。烟酰胺腺嘌呤二核苷酸四唑还原酶染色显示深色染色的肌纤维增多，表明木胸严重程度高。在木胸严重的病例中，线粒体肿胀，木胸严重组肿胀程度最高，正常胸组肿胀程度最低。木胸严重组织中线粒体抗氧化酶基因超氧化物歧化酶1和超氧化物歧化酶2的表达水平显著低于正常组织。这些结果表明，当本应恒定的肌纤维中活性氧水平升高时，线粒体稳态无法维持，细胞各种膜的损伤水平增加，导致正常生理功能紊乱。
