Abstract
Cadmium (Cd), a non-biodegradable contaminant in freshwater ecosystems, can pose a serious threat to aquatic animals at high levels. In this study, the Cd toxicokinetics and the immune and antioxidant defense were explored in Procambarus clarkii exposed to different levels of Cd (0, 0.1, 1.0mg Cd/L) or treated with 1.0mg Cd/L and dietary Bacillus subtilis supplementation (1 × 107cfu/g). Results from the 21-day uptake and depuration experiment revealed that Cd exposure elicited a dose- and time-dependent uptake in all crayfish tissues, and the rank order of Cd concentration was gill > hepatopancreas > exoskeleton > muscle. The one-compartment model demonstrated that gills had the highest uptake rate (ku) value after Cd aqueous exposure and the ku and elimination rate (kd) values in gill, hepatopancreas, and exoskeleton of the group with 1.0mg Cd/L were higher than those of the group at alow Cd concentration (0.1mg Cd/L). However, B. subtilis could decrease Cd ku and increase Cd kd in hepatopancreas, resulting in the reduction of bioconcentration factors (BCF), steady-state concentrations (Css), and biological half-life (Tb1/2). A positive correlation was found between aqueous Cd concentration and the severity of hepatopancreas histopathological injury, while B. subtilis could ameliorate the pathological damage in the high Cd group. Similarly, aqueous exposure to Cd elevated malonaldehyde (MDA) content and suppressed the activities of lysozyme (LZM), acid phosphatase (ACP) in hepatopancreas and alkaline phosphatase (AKP) in hemolymph. The activities of superoxide dismutase (SOD) and catalase (CAT) in hepatopancreas were also inhibited. Nevertheless, they were all recovered with the dietary addition of B. subtilis. In conclusion, our results indicated that exposure to Cd significantly increased Cd accumulation and toxic damages in crayfish hepatopancreas, while dietary administration of B. subtilis to crayfish significantly decreased Cd accumulation and improved the immune and antioxidant defense, leading to the prevention in toxic effects of Cd.
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