Effect of starvation and refeeding on reactive oxygen species, autophagy and oxidative stress in Chinese perch ( Siniperca chuatsi ) muscle growth
Effect of starvation and refeeding on reactive oxygen species, autophagy and oxidative stress in Chinese perch ( Siniperca chuatsi ) muscle growth
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DOI：
10.1111/jfb.15081
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Jianshe Zhang
中科院分区：
文献类型：
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作者：
Ping Wu;Lin Chen;Jia Cheng;Yaxiong Pan;Xin Zhu;Wuying Chu;Jianshe Zhang
In skeletal muscle, autophagy regulates the development and growth of muscle fibers and maintains the normal muscle metabolism. Under starvation and refeeding conditions, the effect of reactive oxygen species (ROS) levels on skeletal muscle autophagy is still unclear, although the excessive accumulation of ROS has been shown to increase autophagy in cells. The purpose of this study was to explore the effects of starvation and diet after starvation on the autophagy of adult Chinese perch muscle, and to determine the level of ROS in the muscle. We performed zero (NC), three, and seven starvation treatments on adult Chinese perch, and returned to normal feeding for three days after being starved for seven days. In the muscles of the adult Chinese perch muscle after three days of starvation, the autophagy marker protein LC3 and the number of autophagosomes remained basically the same as those in the normal feeding situation. However, upon starvation for seven days, the mitochondrial autophagy was sensitive and the number of autophagosomes increased, but the antioxidant-related molecules (malondialdehyde (MDA), catalase (CAT), glutathione S-transferase (GST), glutathione (GSH), and anti-superoxide anion (ASA) decreased and the accumulation of ROS was obvious. In addition, the extended starvation time also increased the level of LC3 protein. however, by refeeding for the recovery after starvation this nutritional stress resulted in a decrease in ROS levels and a partial restoration of antioxidant enzyme activity. Our data showed that in the adult Chinese perch muscle, starvation could reduce the antioxidant activity through the accumulation of ROS, and that the number of the autophagosomes continues to increase. Refeeding after starvation could effectively compensate for the level of ROS and to restore the mRNA abundance of antioxidant genes and the activity of antioxidant enzymes to reduce autophagy, and to improve feed efficiency. Further research should optimize starvation conditions to reduce autophagy in muscles and to maintain normal muscle metabolism. This article is protected by copyright. All rights reserved.
