The impact of menthol essential oil against inflammation, immunosuppression, and histopathological alterations induced by chlorpyrifos in Nile tilapia.

Chlorpyrifos (CPF) is one of the predominant water pollutants associated with inflammation and immunodepression in aquatic animals. In this study, menthol oil (MNT) impacted the immunity, antioxidative, and anti-inflammatory responses against CPF toxicity in Nile tilapia. Fish fed two diets with or without MNT and placed in four groups (control, CPF, MNT, and CPF/MNT). After 30 days, fish fed MNT displayed higher growth performance and lower FCR than CPF-intoxicated fish without feeding MNT (P < 0.05). The survival rate of fish was reduced in the CPF group without MNT feeding (P < 0.05). Blood Hb, PCV, RBCs, and WBCs were decreased in fish by CPF toxicity, while the highest Hb, PCV, RBCs, and WBCs were observed in fish fed MNT followed by those fed the control without CPF toxicity (P < 0.05). Fish fed MNT had the highest total protein, albumin, and globulin, as well as the lowest urea, bilirubin, and creatinine after 15 and 30 days. However, fish under CPF toxicity had the most inferior total protein, albumin, and globulin, as well as the highest urea, bilirubin, and creatinine among the groups (P < 0.05). The enzyme activities of ALP and ALT displayed low levels by MNT with or without CPF exposure than fish fed without MNT with or without CPF exposure after 15 and 30 days (P < 0.05). The lysozyme and phagocytic activities displayed reduced levels by CPF without MNT feeding after 15 and 30 days, while increased activities were noticed by MNT feeding without CPF toxicity followed by fish fed MNT with CPF toxicity (P < 0.05). The transcription of CAT and GPX genes displayed upregulated levels in tilapia fed MNT and exposed to CPF (P < 0.05). Also, CPF toxicity increased the transcription of the IFN-γ gene but decreased the IL-8 and IL-1ß genes. The transcription of HSP70 displayed lower levels (P < 0.05) by CPF without supplementing MNT than fish fed MNT and exposed to CPF. Histopathological analysis revealed that inflammation existed in the liver, gills, and intestine of tilapia due to CPF toxicity while MNT protected tissues from inflammation. To conclude, MNT activated the immunity, antioxidative, and anti-inflammatory responses of Nile tilapia under CPF toxicity.

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-γ, and IL-8 genes. Fish of the CPF group exhibited the lowest IL-1ß, while fish of the MOS/CPF group showed upregulated IL-1ß. 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.