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Enhanced uptake of BPA in the presence of nanoplastics can lead to neurotoxic effects in adult zebrafish
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Researchers found that nanoplastics amplify bisphenol A (BPA) accumulation in zebrafish tissues by 2- to 2.6-fold and that co-exposure enhances neurotoxic effects — including myelin disruption and dopaminergic system changes — beyond what either contaminant causes alone.
Plastic particles have been proven to be abundant in the aquatic environment, raising concerns about their potential toxic effects. In the present study, we determined the bioaccumulation potential of bisphenol A (BPA) in adult zebrafish (Danio rerio) in the absence and presence of nano-sized plastic particles (nanoplastics, NPPs). Results show that BPA can accumulate in the viscera, gill, head and muscle of zebrafish with 85, 43, 20, and 3μg/g ww after 1d exposure. NPPs were also found to accumulate in different tissues of the fish. Relative equilibrium was reached after 1d exposure in different tissues with 39 to 636mg/kg ww. Co-exposure of NPPs and BPA led to a 2.2 and 2.6-fold significant increment of BPA uptake in the head and viscera, if compared with BPA alone treatment after 3d exposure. As such, we further investigated several neurotoxic biomarker alterations in the fish head. It was found that either BPA or NPPs can cause myelin basic protein (MBP)/gene up-regulation in the central nervous system (CNS); meanwhile, both contaminants exhibited significant inhibition of acetylcholinesterase (AChE) activity, which is a well-known representative biomarker for neurotoxicity. Moreover, for the co-exposure treatment, biomarkers of myeline and tubulin protein/gene expressions, dopamine content, and the mRNA expression of mesencephalic astrocyte derived neurotrophic factor (MANF) were all significantly up-regulated, suggesting that an enhanced neurotoxic effects in both CNS and dopaminergic system occurred. However, AChE activity was no more inhibited in the co-exposure treatment, which implies that solely AChE measurement may not be sufficient to identify neurotoxic effects in the cholinergic system. Overall, the present study demonstrates that the presence of NPPs can increase BPA bioavailability and cause neurotoxicity in adult zebrafish.
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Researchers found that when zebrafish larvae were exposed to both polystyrene nanoplastics and the toxic chemical PCB-153 together, the neurological damage was significantly worse than from either pollutant alone. The combined exposure caused hyperactive swimming behavior and suppressed immune, brain, and detoxification pathways at the genetic level. This is concerning because nanoplastics and persistent organic pollutants frequently co-exist in the environment, meaning their real-world health effects on aquatic life and humans may be greater than studies of single pollutants suggest.
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