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Nano-plastics and gastric health: Decoding the cytotoxic mechanisms of polystyrene nano-plastics size
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Researchers examined how different sizes of polystyrene nanoplastics affect human stomach cells in the laboratory. They found that smaller nanoplastics were more readily taken up by the cells and caused greater damage, including increased oxidative stress and reduced cell survival. The study suggests that nanoplastic particle size plays a critical role in determining their potential impact on gastrointestinal health.
Gastrointestinal diseases exert a profound impact on global health, leading to millions of healthcare interventions and a significant number of fatalities annually. This, coupled with escalating healthcare expenditures, underscores the need for identifying and addressing potential exacerbating factors. One emerging concern is the pervasive presence of microplastics and nano-plastics in the environment, largely attributed to the indiscriminate usage of disposable plastic items. These nano-plastics, having infiltrated our food chain, pose a potential threat to gastrointestinal health. To understand this better, we co-cultured human gastric fibroblasts (HGF) with polystyrene nano-plastics (PS-NPs) of diverse sizes (80, 500, 650 nm) and meticulously investigated their cellular responses over a 24-hour period. Our findings revealed PS particles were ingested by the cells, with a notable increase in ingestion as the particle size decreased. The cellular death induced by these PS particles, encompassing both apoptosis and necrosis, showcased a clear dependence on both the particle size and its concentration. Notably, the larger PS particles manifested more potent cytotoxic effects. Further analysis indicated a concerning reduction in cellular membrane potential, alongside a marked increase in ROS levels upon PS particles exposure. This suggests a significant disruption of mitochondrial function and heightened oxidative stress. The larger PS particles were especially detrimental in causing mitochondrial dysfunction. In-depth exploration into the PS particles impact on genes linked with the permeability transition pore (PTP) elucidated that these PS particles instigated an internal calcium rush. This surge led to a compromise in the mitochondrial membrane potential, which in tandem with raised ROS levels, further catalyzed DNA damage and initiated cell death pathways. In essence, this study unveils the intricate mechanisms underpinning cell death caused by PS particles in gastric epithelial cells and highlighting the implications of PS particles on gastrointestinal health. The revelations from this research bear significant potential to shape future healthcare strategies and inform pertinent environmental policies.
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Researchers evaluated the uptake and toxicity of polystyrene micro- and nanoplastics in human gastric cells, comparing different sizes and surface treatments. The study found that smaller 50-nanometer particles were taken up at significantly higher rates, with positively charged aminated particles being the most toxic, causing cytotoxicity at lower concentrations and higher rates of cell death.
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Researchers studied how human intestinal Caco-2 cells take up polystyrene plastic particles of five different sizes ranging from 300 nanometers to 6 micrometers. The study found that smaller particles were taken up at higher rates and that co-exposure with bisphenol A increased cellular toxicity, suggesting that nanoscale plastics may pose a greater risk to human intestinal cells than larger microplastics.
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