Histidine Deficiency Inhibits Intestinal Antioxidant Capacity and Induces Intestinal Endoplasmic-Reticulum Stress, Inflammatory Response, Apoptosis, and Necroptosis in Largemouth Bass (Micropterus salmoides)
文献类型: 外文期刊
作者: Liang, Hualiang 1 ; Xu, Pao 1 ; Xu, Gangchun 1 ; Zhang, Lin 1 ; Huang, Dongyu 2 ; Ren, Mingchun 1 ; Zhang, Lu 3 ;
作者机构: 1.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Integrated Rice Fish Farming Ecol, Minist Agr & Rural Affairs, Wuxi 214081, Peoples R China
2.Nanjing Agr Univ, Wuxi Fisheries Coll, Wuxi 214081, Peoples R China
3.Tongwei Co Ltd, Hlth Aquaculture Key Lab Sichuan Prov, Chengdu 610093, Peoples R China
关键词: histidine deficiency; juvenile largemouth bass (Micropterus salmoides); antioxidant capacity; endoplasmic-reticulum stress; inflammation
期刊名称:ANTIOXIDANTS ( 影响因子:7.675; 五年影响因子:7.886 )
ISSN:
年卷期: 2022 年 11 卷 12 期
页码:
收录情况: SCI
摘要: This 56-day study aimed to evaluate the effects of histidine levels on intestinal antioxidant capacity and endoplasmic-reticulum stress (ERS) in largemouth bass (Micropterus salmoides). The initial weights of the largemouth bass were (12.33 +/- 0.01) g. They were fed six graded levels of histidine: 0.71% (deficient group), 0.89%, 1.08%, 1.26%, 1.48%, and 1.67%. The results showed that histidine deficiency significantly suppressed the intestinal antioxidant enzyme activities, including SOD, CAT, GPx, and intestinal level of GSH, which was supported by significantly higher levels of intestinal MDA. Moreover, histidine deficiency significantly lowered the mRNA level of nrf2 and upregulated the mRNA level of keap1, which further lowered the mRNA levels of the downstream genes sod, cat, and gpx. Additionally, histidine-deficiency-induced intestinal ERS, which was characterized by activating the PEPK-signalling pathway and IRE1-signalling pathway, including increased core gene expression of pepk, grp78, eif2 alpha, atf4, chop alpha, ire1, xbp1, traf2, ask1, and jnk1. Dietary histidine deficiency also induced apoptosis and necroptosis in the intestine by upregulating the expressions of proapoptotic genes, including caspase 3, caspase 8, caspase 9, and bax, and necroptosis-related genes, including mlkl and ripk3, while also lowering the mRNA level of the antiapoptotic gene bcl-2. Furthermore, histidine deficiency activated the NF-kappa B-signalling pathway to induce an inflammatory response, improving the mRNA levels of the proinflammatory factors tnf-alpha, hepcidin 1, cox2, cd80, and cd83 and lowering the mRNA levels of the anti-inflammatory factors tgf-beta 1 and ikb alpha. Similarly, dietary histidine deficiency significantly lowered the intestinal levels of the anti-inflammatory factors TGF-beta and IL-10 and upregulated the intestinal levels of the proinflammatory factor TNF-alpha, showing a trend similar to the gene expression of inflammatory factors. However, dietary histidine deficiency inhibited only the level of C3, and no significant effects were observed for IgM, IgG, HSP70, or IFN-gamma. Based on the MDA and T-SOD results, the appropriate dietary histidine requirements of juvenile largemouth bass were 1.32% of the diet (2.81% dietary protein) and 1.47% of the diet (3.13% dietary protein), respectively, as determined by quadratic regression analysis.
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