Polystyrene nanoplastics exposure causes inflammation and death of esophageal cell

Abstract

Nanoplastics (NPs) are widely detected in food and drinking water, and human exposure to NPs is ubiquitous. The digestive tract is the main route of exposure to NPs in humans, and the esophagus is one of the main target organs for NPs exposure. However, the toxicological effects of polystyrene nanoplastics (PS-NPs) on the esophagus are not fully understood. Here, we used two esophageal cell lines as models to explore the effects of NPs exposure on esophageal cells and the underlying molecular mechanisms. Western blot analysis, indirect immunofluorescence assay, and enzyme-linked immunosorbent assay revealed that NPs exposure caused inflammatory responses and cell death. Mechanistic investigations showed that PS-NPs exposure induced iron overload in esophageal cells, leading to the accumulation of mitochondrial reactive oxygen species and promoting inflammatory responses and cell death. Additionally, PS-NPs treatment suppressed mitochondrial autophagy, which exacerbated NP-induced cell inflammation and death. Collectively, our experimental findings provide new evidence for the toxicological effects of PS-NPs and offer new insights and avenues for future research.

Keywords

• Nanoplastics
• Inflammation
• Esophageal cells
• Iron overload
• Cell death