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Polystyrene micro(nano)plastics damage the organelles of RBL-2H3 cells and promote MOAP-1 to induce apoptosis
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Researchers exposed immune cells to polystyrene particles of different sizes and found that the particles caused oxidative stress, damaged mitochondria and lysosomes, and triggered programmed cell death. The study identified a specific molecular mechanism involving the MOAP-1 protein that drives microplastic-induced cell death, with 50-nanometer particles causing the most severe effects.
The ubiquity of microplastics increases the exposure risks and health threats to humans. In this study, rat basophilic leukemia (RBL-2H3) cells were exposed to polystyrene particles (PS-particles) of 50 nm, 500 nm and 5 µm to investigate organelle damage and the mechanism of cell death. PS-particles induced oxidative stress, which in turn led to mitochondrial and lysosomal damage, arrested the cell cycle in the G0/G1 phase, and finally caused apoptosis. Anti-apoptotic genes (Bcl-2) were down regulated, and pro-apoptotic genes (Bax) and a key gene (caspase-3) in apoptosis were upregulated. The molecular mechanism of apoptosis was further explored via the combination of transcriptome sequencing, RT-qPCR verification and small interfering RNA (siRNA) technology. The modulator of apoptosis-1 (MOAP-1) was significantly upregulated, and apoptosis was abolished by knocking down MOAP-1. This finding clarifies that PS-particles promote MOAP-1 to induce apoptosis. Hence, PS-particles may promote the binding of MOAP-1 and Bax, which ultimately activates caspase-3 and causes apoptosis through the mitochondrial pathway. The 50-nm PS-particles resulted in the most serious mitochondrial damage and apoptosis. Eventually, PS-particles cause oxidative stress, damage organelles and induce apoptosis by promoting MOAP-1. Altogether, our study emphasizes the need to assess the cytotoxicity of micro(nano)plastics and helps to predict the health risks.
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