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Polystyrene Nanoplastics and Cadmium Co-Exposure Accelerates Mitochondrial Autophagy Mediated by HSP60–SIRT3–SOD 2 Signaling Pathway in Primary Duck Embryo Hepatocytes
Summary
Scientists found that when tiny plastic particles and the toxic metal cadmium are combined, they cause more damage to liver cells than either pollutant alone. The plastic particles help cadmium get into cells more easily, leading to harmful changes in the cell's powerhouses (mitochondria) and increased cell death. While this study used duck cells, it suggests that the growing presence of microplastics in our environment could make heavy metal pollution more dangerous to human health.
Microplastics (MPs) in the environment frequently act as a medium to adsorb heavy metals and antibiotics. This combined exposure often has a greater effect on animal toxicity than exposure alone. However, there is a paucity of research focusing on the combined toxicity of nanoplastics (NPs) and heavy metals when coexposed to hepatocytes in poultry. In this study, the effects of PS-NPs (0.08 μm, 10 μg/mL) and cadmium chloride (CdCl2) (4 μg/mL) on duck hepatocytes and their mechanisms were observed using primary duck embryo hepatocytes (PDEH) cells as an in vitro model. The results demonstrated that Cd exposure exacerbated the accumulation of PS-NPs in PDEH cells, likely due to the formation of pores on the cell membrane surface. The addition of the antioxidant N-Acetyl-l-cysteine (NAC) significantly reduced the uptake of PS-NPs by PDEH cells. PDEH cells in the coexposed group exhibited significantly abnormal morphology and diminished cell number and survival rate. Furthermore, exposure to PS-NPs exacerbated Cd-mediated oxidative stress and mitochondrial autophagy damage in duck hepatocytes. The restoration of these injuries was observed in response to intervention with the SIRT3 activator (NRCL, 2 ng/mL). Immunoprecipitation experiments demonstrated that the SIRT3 protein interacted with the SOD2 protein. The present study found that co-exposure of PS-NPs+Cd induced mitochondrial autophagy in PDEH cells, which may be mediated by the HSP60/SIRT3/SOD2 signaling axis. It is hoped that these findings will provide new ideas for combating the mechanism of microplastics and Cd-induced hepatotoxicity in poultry.
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