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Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
OBJECTIVE: To investigate the long-term effects of polystyrene (PS) exposure on acute liver injury. METHODS: The carbon tetrachloride-induced acute injury mouse model was subjected to long-term PS exposure. Pyroptosis was inhibited by knocking out Gsdmd in mice or treating with the Gsdmd inhibitor necrosulfonamide (NSA) to evaluate the effect of PS on liver injury. Kupffer cells were used as a cellular model to examine the effects of PS on cell pyroptosis, lactate dehydrogenase release rate, structural integrity (propidium iodide staining), and inflammatory factor levels. RESULTS: In mice, PS exposure exacerbated acute liver injury, which was mitigated upon Gsdmd knockout (KO) or NSA treatment along with the downregulation of tissue inflammatory response. In vitro studies demonstrated that PS promoted Kupffer cell pyroptosis, which was suppressed upon Gsdmd KO or NSA treatment along with the alleviation of inflammation. CONCLUSION: These results suggest that long-term PS exposure exacerbates acute liver injury by promoting Kupffer cell pyroptosis, which is one of the hepatotoxic mechanisms of PS.
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Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
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Scientists found that tiny plastic particles (microplastics) can damage the liver in fish by triggering inflammation and a type of cell death linked to iron and fat breakdown, essentially causing cells to self-destruct in a harmful way. While this study was done in tilapia, not humans, it adds to growing evidence that the microplastics we're increasingly exposed to through food, water, and air may cause similar organ damage in other animals—including potentially us—making this an important area for future human health research.
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Researchers discovered that polystyrene microplastics trigger liver inflammation by causing immune cells called macrophages to release web-like structures (extracellular traps) that damage surrounding liver cells. The mechanism involves microplastics generating harmful reactive oxygen species inside macrophages, disrupting their internal recycling systems and ultimately causing them to burst, which highlights how microplastics may drive organ inflammation in the body.
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