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Polystyrene Nanoplastics Induce Lipophagy Via the Ampk/Ulk1 Pathway and Block Lipophagic Flux Leading to Lipid Accumulation in Hepatocytes
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Polystyrene nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
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Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
Cellular Uptake and Nuclear Accumulation of Polystyrene Nanoplastics in 3T3 Fibroblasts and Hepatocytes of Rattus norvegicus
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Scientists found that tiny plastic particles called nanoplastics can get inside liver and connective tissue cells from rats, and even sneak into the cell's nucleus, where DNA is stored. Cells exposed to these plastics showed signs of stress and damage, including swelling and higher rates of cell death, suggesting these ultra-small plastic particles may be more harmful than previously thought. While this study used animal cells rather than human cells, it raises important questions about what everyday exposure to nanoplastics (found in food packaging, water, and other sources) might mean for our own cellular health.
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Researchers fed rats a high-fat diet alongside low-dose polystyrene nanoplastics for 90 days and found the nanoplastics unexpectedly reduced liver fat accumulation and inflammation by activating AMPK-mediated lipophagy, revealing a context-dependent interaction where low-dose plastic exposure can trigger a stress-adaptation response that partially counteracts diet-induced hepatic injury.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
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Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Disruption of lipid metabolism under plastic siege: Unraveling the toxic mechanisms of microplastics and nanoplastics
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