Hunan Provincial Key Laboratory of Nutrition and Quality Control of Aquatic Animals, College of Biological and Environmental Engineering, Changsha University, Changsha, China.
College of Chemistry and Food Engineering, Changsha University of Science & Technology, Changsha, China.
Sci Rep. 2021 Feb 11;11(1):3657. doi: 10.1038/s41598-021-83388-6.
Muscle is an important structural tissue in aquatic animals and it is susceptible to bacterial and fungal infection, which could affect flesh quality and health. In this study, Chinese soft-shelled turtles were artificially infected with two pathogens, Proteus vulgaris and Elizabethkingia meningoseptica and the effects on muscle nutritional characteristics, oxidative stress and autophagy were assayed. Upon infection, the muscle nutritional composition and muscle fiber structure were notably influenced. Meanwhile, the mRNA expression of Nrf2 was down-regulated and Keap1 up-regulated, thus resulting in a decrease in antioxidant capacity and oxidative stress. However, with N-acetylcysteine treatment, the level of oxidative stress was decreased, accompanied by significant increases in antioxidant enzyme activities and the mRNA levels of SOD, CAT, GSTCD, and GSTO1. Interestingly, there was a significant increase in autophagy in the muscle tissue after the pathogen infection, but this increase could be reduced by N-acetylcysteine treatment. Our findings suggest that muscle nutritional characteristics were dramatically changed after pathogen infection, and oxidative stress and autophagy were induced by pathogen infection. However, N-acetylcysteine treatment could compromise the process perhaps by decreasing the ROS level and regulating Nrf2-antioxidant signaling pathways.
肌肉是水生动物的重要结构组织,容易受到细菌和真菌感染,这可能会影响肉质和健康。在这项研究中,我们人工感染中华鳖两种病原体,普通变形杆菌和脑膜败血伊丽莎白菌,检测其对肌肉营养特性、氧化应激和自噬的影响。感染后,肌肉营养成分和肌肉纤维结构明显受到影响。同时,Nrf2 的 mRNA 表达下调,Keap1 上调,导致抗氧化能力和氧化应激降低。然而,用 N-乙酰半胱氨酸处理后,氧化应激水平降低,同时抗氧化酶活性和 SOD、CAT、GSTCD 和 GSTO1 的 mRNA 水平显著升高。有趣的是,病原体感染后肌肉组织中自噬明显增加,但 N-乙酰半胱氨酸处理可减少自噬增加。我们的研究结果表明,病原体感染后肌肉营养特性发生显著变化,病原体感染诱导氧化应激和自噬。然而,N-乙酰半胱氨酸处理可能通过降低 ROS 水平和调节 Nrf2-抗氧化信号通路来影响这一过程。