Effects of saline-alkali stress on the tissue structure, antioxidation, immunocompetence and metabolomics of Eriocheir sinensis

Saline-alkali water resources are abundant and widely distributed in China. The effective utilization of saline-alkali water resources by fishery is of great significance to enhance the aquatic product economy and restore the ecology of saline-alkali environments. Eriocheir sinensis is a saline-alkali water-suitable species. To explore its physiological response to saline-alkali stress, the hepatopancreas tissue structure, antioxidation, immunocompetence and metabolomics were investigated after 96 h of gradient saline-alkali treatment. The results confirmed the hepatopancreas damage through tissue sectioning, abnormal enzyme activity (aspartate transaminase (AST), alanine aminotransferase (ALT)) and aberrant malondialdehyde (MDA) content. The activity of superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (T-AOC) was significantly upregulated (p < 0.05), which was followed by a decrease trend, indicating the enhancement of antioxidant capacity in response to the stress. Strengthened immunocompetence in response to saline-alkali toxicity was shown in the gradual increase of immune enzyme activity (acid phosphatase (ACP) and alkaline phosphatase (AKP)) and the upregulated expression of immune genes (hsp 70, hsp 90, proPO and toll). Among the differential metabolites quantified by metabolomics, small peptides were significantly downregulated (p < 0.05), and acylcarnitines were obviously upregulated (p < 0.05), indicating that saline-alkali toxicity inhibited protein catabolism and stimulated the mobilization of energy reserves. Metabolic pathways enriched through the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis suggested that Eriocheir sinensis activated different mechanisms in response to various degrees of stress, such as “ABC transporters” and “purine metabolism” in response to low saline-alkali stress, while “pyrimidine metabolism” and “beta-alanine metabolism” to high saline-alkali stress.