The effect of mannanoligosaccharide on the growth performance, histopathology, and the expression of immune and antioxidative related genes in Nile tilapia reared under chlorpyrifos ambient toxicity

The role of mannanoligosaccharide (MOS) in reducing the adverse effects of chlorpyrifos (CPF) toxicity in tilapia was evaluated in the present study. Fish were allotted into four groups and fed the basal diet or MOS and exposed to CPF (control, CPF, MOS, and MOS/CPF) for 30 days. Fish fed MOS revealed higher growth and survival rates and lower FCR than CPF-intoxicated fish (P < 0.05). The Hb, PCV, RBCs, and WBCs variables were lowered by CPF toxicity and increased by MOS (P < 0.05). The values of total protein (sTP), albumin (ALB), globulin (GLB), lysozyme (LZM), and phagocytic activities (PA) decreased whereas, ALP, ALT, AST, urea, bilirubin (BIL), and creatinine (CR) were increased by CPF toxicity. However, dietary MOS increased the sTP, ALB, GLB, LZM, and PA and decreased the ALP, ALT, AST, BIL, and CR. The PA and phagocytic index displayed higher levels by MOS feeding than the other groups (P < 0.05). The lowest mRNA level of GPX1 (cellular GPX) gene was observed in fish of the CPF group, while the highest level was shown in the MOS/CPF group (P < 0.05). Fish in the control and CPF groups displayed downregulated CAT whereas the expression of GPX and CAT genes was higher in fish of the MOS/CPF group than fish in the MOS group (P < 0.05). MOS upregulated the expression of HSP70 gene with CPF toxicity. Fish of the CPF and MOS/CPF groups displayed upregulated CASP3, IFN-gamma, and IL-8 genes. Fish of the CPF group exhibited the lowest IL-1 beta, while fish of the MOS/CPF group showed upregulated IL-1 beta. The intoxication with CPF induced histopathological inflammations in the gills, intestine, and liver tissues, while dietary MOS protected against inflammation. In summary, dietary MOS is recommended as an immunostimulant to counteract the inflammatory impacts of waterborne CPF toxicity in Nile tilapia.