Abstract

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.