Dietary threonine influences antioxidant capacity and immune status in juvenile largemouth bass (Micropterus salmoides)

As a restricted amino acid, threonine (Thr) deficiency reduces antioxidant and immune capacity in fish. In the present study, six diets containing different Thr levels (1.39 %, 1.71 %, 1.95 %, 2.28 %, 2.58 %, and 2.65 %) were fed to largemouth bass (15±0.1 g) for 60 days. The present results showed that neither growth nor whole-body composition was affected by different Thr levels. And low dietary Thr levels (1.39 %) significantly decreased serum total protein (TP) and albumin (ALB) levels, but increased alkaline phosphatase (ALP) levels. And 1.39 % Thr diet significantly decreased liver catalase (CAT) activity but increased malonaldehyde (MDA) levels, and the maximum total antioxidant capacity (T-AOC) was observed in response to the 1.95 % Thr diet. Liver proapoptotic factors (bax and caspase9) were significantly elevated in fish fed the 1.39 % Thr diet. The nuclear factor κB (nf-κb) and the NF-κB-mediated inflammatory cytokines were significantly increased in fish fed the 1.39 % Thr diet. The mRNA levels of protein kinase R (PKR)-like endoplasmic reticulum kinase (perk), eukaryotic translation initiation factor 2 (eif2α), activating transcription factor 4 (atf4), and C/EBP-homologous protein (chop), which are factors in the PERK/ATF4/CHOP pathway, one of the unfolded protein response (UPR) signaling pathways, were significantly increased by the 1.39 % Thr diet. The present study showed that low dietary Thr levels caused oxidative damage, reduced immunity, might affected PERK-ATF4-CHOP signaling to induce apoptosis, and via NF-κB signaling to trigger an inflammatory response in largemouth bass. Based on the TP, ALB, CAT, and MDA levels, the dietary Thr requirements for juvenile largemouth bass were estimated to be 2.18 %, 2.29 %, 1.92 %, and 1.88 %. Furthermore, these findings provided a new perspective that low dietary amino acid levels may trigger apoptosis and inflammatory responses in fish through the UPR signaling pathway.