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Polystyrene microplastics induce apoptosis via ROS-mediated p53 signaling pathway in zebrafish
Summary
Researchers discovered that polystyrene microplastics trigger programmed cell death in zebrafish gills through a molecular pathway involving reactive oxygen species and the p53 gene. The microplastics caused dose- and time-dependent oxidative damage, inflammation, and physical injury to gill tissue at concentrations as low as 10 micrograms per liter. The study provides molecular-level evidence explaining how microplastic exposure can harm aquatic organisms.
Microplastic (MP) pollution is ubiquitous and has become an emerging threat to aquatic biota. Recent scientific reports have recorded their toxic impacts at the cellular and organism levels, but the underlying molecular mechanism of their toxicity remains unclear. The present study elucidates an array of molecular events underlying apoptosis in the gills of polystyrene microplastics (PS-MPs) exposed zebrafish (Danio rerio). PS-MPs at different concentrations (10 and 100 μg L) induced the reactive oxygen species (ROS) generation, in turn affecting the oxidative and immune defense mechanism. The expression profile of antioxidant genes cat, sod1, gpx1a and gstp1 were altered significantly. PS-MPs also significantly inhibited the neurotransmission in zebrafish. In addition, the PS-MPs exposure upregulated the expression of p53, gadd45ba, and casp3b resulting in apoptosis. We demonstrate that PS-MPs significantly upregulate the transcriptional pattern of tnfa and ptgs2a which are essential gene markers in inflammatory mechanism. Further, the oxidative damage induced by PS-MPs exposure could lead to cytological damage resulting in altered lamellar structures, capillary dilation, and necrosis in gill histomaps. In conclusion, the findings of this work strongly suggest that PS-MPs induce dose-and time-dependent ROS mediated apoptotic responses in zebrafish. Furthermore, the physiological responses observed in the gills correlate with the above observations and helps in unravelling the potential molecular mechanism underpinning the PS-MPs toxicity in zebrafish.
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