Phosphate, as the main nutrient factor of lake eutrophication brought by pollutants discharged from agriculture and industry, is always considered to be a low-toxicity substance to aquatic animals. But the toxicity mechanism is unclear, and published information is limited. In this study, a 96 h acute stress experiment was conducted on juvenile turbot (Scophthalmus maximus) with 0, 10, and 60 mg/L phosphate solutions. Metabonomic analysis revealed that low-dose phosphate (10 mg/L) disrupted glycerophospholipid, purine, and glycolipid metabolism, as well as the tricarboxylic acid (TCA) cycle in juveniles, even at 96 h of stress, which may lead to cell structure damage and signal recognition disorder between cells. Upregulated key genes in the main glycerophospholipid metabolic pathways, which matched the results of the metabolomic study, were detected. Furthermore, low-dose phosphate (10 mg/L) induced oxidative stress and immunotoxicity in fish, resulting in the raising of relevant genes expression such as cat and sod in liver and kidney. In addition, all phosphate-treated groups had induced lesions on gill tissue, as evidenced by pathological observations. In this study on toxic effects on and mechanism of phosphate in aquatic animals using metabolomics, gene expression, and histopathology, we confirm that acute low-dose phosphate could disrupt glycerophospholipid metabolism and induce stress in juvenile turbot. This can provide advice on the amount of phosphate accumulation for marine fish farming and on protecting species diversity and marine ecosystem from the point of view of phosphate toxicity to marine animals.
Keywords: Gene expression; Histopathological damage; Metabolomics; Phosphate; Toxicity.
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