Effects of dietary astaxanthin on the growth, innate immunity and antioxidant defence system of Paramisgurnus dabryanus. (28th August 2020)

• Record Type: Journal Article
• Authors: Chen, Xiu‐Mei; Gao, Chun‐Shan; Du, Xiao‐Yan; Yao, Jin‐Ming; He, Fei‐Fei; Niu, Xiao‐Tian; Wang, Gui‐Qin; Zhang, Dong‐Ming
• Is Part Of: Aquaculture nutrition. Volume 26:Number 5(2020)
• Page Start: 1453
• Page End: 1462
• Publication Date: 2020-08-28
• Subjects: antioxidant defence system -- astaxanthin -- growth -- innate immunity -- Paramisgurnus dabryanus; Aquaculture -- Periodicals; Aquatic animals -- Feeding and feeds -- Periodicals; Fishes -- Feeding and feeds -- Periodicals; 639.3
• DOI: 10.1111/anu.13093
• Languages: English
• ISSNs: 1353-5773

Abstract

Abstract: The effects of astaxanthin supplementationon the growth, innate immunity and antioxidant defence system of loach ( Paramisgurnus dabryanus ) were investigated in this study. A total of 450 fish (initial average weights of 3.00 ± 0.10 g) were fed five diets with graded levels of astaxanthin (0.00, 50.00, 100.00, 150.00 and 200.00 mg/kg) for 56 days. The results showed that astaxanthin supplementation significantly stimulated the growth (FBW, WG, FER, HSI), innate immunity (AKP activity in the hepatopancreas, intestinal tract, muscle and skin and LZM activity in the hepatopancreas, intestinal tract and skin), antioxidant ability (T‐SOD, GSH‐PX and CAT activities and T‐AOC, GSH and MDA contents in the hepatopancreas, intestinal tract, muscle and skin) of loach. Moreover, dietary astaxanthin supplementation significantly up‐regulated the relative mRNA levels of Nrf2 and Maf, and down‐regulated the relative mRNA level of Keap1 in the hepatopancreas when the supplementation levels of astaxanthin were 50–200 mg/kg. In conclusion, the diets with 100–151.06 mg/kg astaxanthin supplementation were optimal for loach, which based on the growth, immunity and antioxidant‐related indicators, and the astaxanthin supplementation regulated the antioxidant ability partially referring to Keap1‐Nrf2 signallings.