AI Article Synopsis

  • - The 56-day study assessed how different levels of histidine in the diet affect antioxidant capacity and endoplasmic-reticulum stress (ERS) in largemouth bass, revealing that histidine deficiency reduced important antioxidant enzymes and increased markers of oxidative stress.
  • - Findings indicated that a lack of histidine led to intestinal ERS, apoptosis, and inflammation, as evidenced by changes in mRNA levels of various genes related to stress, apoptosis, and proinflammatory responses.
  • - The study concludes that maintaining adequate histidine levels in the diet is crucial for the overall health and intestinal function of largemouth bass, as deficiency impacts both oxidative stress and immune responses.

Article Abstract

This 56-day study aimed to evaluate the effects of histidine levels on intestinal antioxidant capacity and endoplasmic-reticulum stress (ERS) in largemouth bass (). 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 and upregulated the mRNA level of , which further lowered the mRNA levels of the downstream genes , and . 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 , , eif2α, , , , , , and . Dietary histidine deficiency also induced apoptosis and necroptosis in the intestine by upregulating the expressions of proapoptotic genes, including , , , and and necroptosis-related genes, including and , while also lowering the mRNA level of the antiapoptotic gene . Furthermore, histidine deficiency activated the NF-κB-signalling pathway to induce an inflammatory response, improving the mRNA levels of the proinflammatory factors , , , , and and lowering the mRNA levels of the anti-inflammatory factors and . Similarly, dietary histidine deficiency significantly lowered the intestinal levels of the anti-inflammatory factors TGF-β and IL-10 and upregulated the intestinal levels of the proinflammatory factor TNF-α, 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-γ. 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9774248PMC
http://dx.doi.org/10.3390/antiox11122399DOI Listing

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