Ellagic acid can mitigate chronic ammonia stress-induced adverse effects through the augmentation of liver autophagy in yellow catfish (Pelteobagrus fulvidraco)

Abstract

The toxicity of ammonia to the majority of fish species is well-known, however, its harmful impact can be mitigated through nutritional intervention. The aim of this study was to investigate whether dietary supplementation of ellagic acid (EA) can mitigate the toxicity of chronic ammonia stress on yellow catfish. Three groups of yellow catfish were fed diets containing different concentrations of EA (0.00, 0.02, and 0.20%) for a duration of 56 days. Additionally, the fish were exposed to three different levels of ammonia (0.00, 2.50, and 25.00 mg/L total ammonia nitrogen) in order to assess any potential interactions. The results showed that ammonia toxicity could affect growth (weight gain rate and specific growth rate were decreased but feed conversion ratio declined), leads to oxidative stress (total antioxidant capacity, superoxide dismutase, and catalase decreased but H2O2 content increased), and physiological function damage (total cholesterol, total protein, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase increased). Additionally, autophagy (becn1, atg3, atg4a, atg7, lc3a, and sqstm1), apoptosis (tgf-β, smad 2, caspase 3, caspase 9, and baxa), inflammation (TNF-α, IL-1β, and Myd88) related genes were up-regulated while myogenic regulatory factors (myod, myf5, myog, and igf) were down-regulated by ammonia. The inclusion of dietary EA supplementation has the potential to alleviate the detrimental impact of ammonia poisoning on fish growth, oxidative damage, physiological function impairment, and apoptotic processes by activating autophagy.