| Summary: | An eight-week feeding trial was conducted to determine the optimal dietary histidine requirement of juvenile swimming crab (Portunus trituberculatus). Six isonitrogenous and isolipidic diets (45.0% crude protein and 8.0% crude lipid) were formulated to contain 0.43%, 0.68%, 0.97%, 1.24%, 1.45% and 1.79% histidine, respectively. Each diet was randomly assigned to triplicate groups of 30 juvenile crabs (approximately initial weight 17.63 ± 0.08 g). The results indicated that the highest percent weight gain (PWG) and specific growth rate (SGR) was presented in crabs fed the diet with 1.24% histidine (P < 0.05). Crabs fed the diet with 1.45% histidine showed remarkably higher activities of alanine transaminase (ALT) and aspartate transaminase (AST) in hemolymph than those fed the other diets (P < 0.05). Meanwhile, the concentrations of malondialdehyde (MDA) in hemolymph and hepatopancreas remarkably decreased with dietary histidine levels increasing from 0.43% to 1.79%, and activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC) and hydroxyl radical scavenging activity in hemolymph and hepatopancreas exhibited the significant trend of first increasing to 1.17% histidine and then decreasing (P < 0.05). The concentrations of carnosine significantly increased with the increase of dietary histidine levels (P < 0.05). Moreover, dietary histidine levels could significantly influence the mRNA levels of genes related to TOR pathway such as tor, akt, s6k1, s6, eif4e1a, eif4e2 and eif4e3, and antioxidant such as cat, cMnsod, gpx, trx and prx (P < 0.05). Two slope broken-line model analysis of PWG against the dietary histidine levels indicated that the optimal dietary histidine requirement was estimated to be 1.17% of the dry matter (2.60% of the dietary protein) for juvenile swimming crab. In conclusion, dietary 1.24% histidine can significantly increase the carnosine contents in muscle, hepatopancreas and hemolymph, improve antioxidant performance and activate the TOR signaling pathway.
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