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Polystyrene microplastic exposure induces hepatic damage via immune-modulated autophagy and ferroptosis in Nile tilapia (Oreochromis niloticus)
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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.
Hepatic damage in fish induced by microplastic exposure has garnered increasing concern, yet its molecular mechanisms remain insufficiently elucidated. In this study, 30 days after hatching (dah) Nile tilapia were subjected to sub-chronic exposure to polystyrene microplastics (PS; 100 nm) for 14 days. Histopathological examination revealed evident inflammatory cell infiltration in the livers of PS-exposed fish compared to the control fish. Transmission electron microscopy showed elevated mitochondrial rupture and increased autophagosome formation. Immunofluorescence and Western blot analyses showed upregulated Lc3b and downregulated P62 protein levels, suggesting enhanced hepatic autophagy. Transcriptomic profiling of liver tissues and subsequent KEGG enrichment analysis highlighted significant upregulation of genes involved in the MAPK, NOD-like receptor, Toll-like receptor, and autophagy signaling pathways. Metabolomic profiling indicated notable enrichment in glutathione metabolism, ferroptosis, cysteine and methionine metabolism, and the NOD-like receptor pathway. Integrated transcriptomic and metabolomic KEGG analysis consistently identified ferroptosis as a centrally enriched pathway. Further gene expression and metabolite analyses demonstrated marked upregulation of immune-related genes, autophagy-related genes, and ferroptosis-pathway genes. Concurrently, ferroptosis-related metabolites including glutathione and cysteine were significantly decreased. Meanwhile, levels of lipid metabolites such as 2-oleoylglycerol were also reduced, whereas lipid peroxidation products represented by 4-hydroxynonenal were significantly increased. Additional validation confirmed increased expression of inflammatory factors (il-1β, tgf-β, nlrp3) and altered iron homeostasis in the PS-exposed fish liver. These findings indicate that sub-chronic PS exposure promotes hepatic ferroptosis via immune-mediated activation of autophagy, ultimately leading to liver injury in Nile tilapia. Our study provides novel insights into the mechanisms underlying microplastic-induced tissue damage in aquatic organisms.
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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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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.
Time-dependent biphasic dysregulation of autophagy and innate immunity underlies polystyrene microplastics-induced hepatotoxicity in Nile tilapia
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Researchers tracked Nile tilapia liver responses to polystyrene microplastics over 21 days, revealing a biphasic pattern in which early autophagy induction preceded innate immune activation at 14 days, followed by broad suppression of both pathways by day 21 — with pharmacological autophagy inhibition confirming that autophagy directly triggers the subsequent inflammatory cascade.
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In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
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Gilthead seabream fed polystyrene microplastics for 21 days developed signs of liver damage including fat buildup, inflammation, and oxidative stress -- changes similar to early-stage fatty liver disease. Since fish liver responds to microplastics in ways comparable to mammalian livers, these findings raise concerns about what chronic microplastic exposure might do to liver health in humans and other animals.
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