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Effects of dietary nanoplastics exposure on muscle quality, immunity, antioxidative capacity and digestive gland function of abalone (Haliotis discus hannai)
Summary
Researchers fed abalone different concentrations of polystyrene nanoplastics for 21 days and observed dose-dependent harm across multiple organ systems. The nanoplastics impaired antioxidant defenses, suppressed immune function, degraded muscle texture, and caused fat accumulation and inflammation in the digestive gland. The study suggests that dietary nanoplastic exposure poses significant risks to the health and quality of commercially important shellfish species.
The increasing accumulation of nanoplastics (NPs) in marine environment poses significant ecological and economic risks, particularly for commercially important species such as abalone (Haliotis discus hannai). This study investigated the effects of dietary polystyrene NPs (0,1, 10 and 100 mg/kg) on abalone over a 21-day exposure period, and the groups were designated as control, NPs1, NPs10 and NPs100, respectively. Results demonstrated that NPs impaired antioxidant capacity, as evidenced by elevated malondialdehyde (MDA) levels in cell-free hemolymph (1.83-fold higher in the NPs100 group than in control), together with reduced superoxide dismutase activity, decreased total antioxidant capacity, and inhibition of the Keap1/Nrf2 pathway. Immune suppression was observed through decreased lysozyme and acid phosphatase activities. Muscle texture deterioration was observed (muscle hardness decreased to 0.42-fold of the control level in NPs100 group), which was associated with reduced protein content, inhibition of the mTOR pathway, and upregulation of proteolytic genes (capn1, capn2, ctsl and ctsb). In the digestive gland, NPs induced lipid accumulation (increased to 1.20-fold of the control level in the NPs100 group), accompanied by suppressed lipolysis-related genes (atgl, hsl, cpt-1 and acox) and enhanced lipogenesis-related genes (srebp-1c, acc and scd) expression. Additionally, NPs upregulated inflammation-related genes (myd88, nf-κb, tnf-α and il-17) and apoptosis-related proteins (BAX, CytC and cleaved caspase-3), along with histopathological changes and reduced digestive enzyme activities. These findings indicate that NPs impair abalone health and muscle quality through oxidative stress, metabolic disruption, apoptosis and protein turnover. Primary adverse effects were mainly observed at ≥10 mg/kg after 21 days, with the most pronounced responses at 100 mg/kg. The mTOR, NF-κB, and Bax/caspase-3 signaling pathways were the main targets of the biological effects induced by NPs.
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