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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.
The immunotoxicity of microplastic pollution in aquatic species is an issue of growing concern. However, the time course and mechanistic crosstalk underlying microplastic-induced hepatic injury remain poorly defined. This study examined the temporal hepatic response of Nile tilapia (Oreochromis niloticus) to 100 nm polystyrene microplastics (PS) over a 21-day exposure period, covering acute (7 days) and sub-chronic (14 and 21 days) phases. Histopathological evaluation showed no obvious liver lesions in exposed fish relative to controls at 7 days post-exposure (dpe). In contrast, progressive tissue damage marked by enhanced inflammatory cell infiltration was apparent at 14 and 21 dpe. PS exposure triggered time-dependent oxidative stress, with reactive oxygen species (ROS) and malondialdehyde (MDA) levels significantly increased and superoxide dismutase (SOD) activity decreased at 14 and 21 dpe. Ultrastructural analysis using transmission electron microscopy (TEM) further revealed distinct mitochondrial swelling and a notable increase in autophagosome numbers within hepatocytes at 7 and 14 dpe. Transcriptomic profiling indicated a biphasic dysregulation affecting both autophagy and inflammatory pathways. Specifically, autophagy-related pathways were significantly upregulated by 7 dpe, which preceded the marked activation of innate immune signaling pathways, such as NOD-like receptors (NLR) and mitogen-activated protein kinase (MAPK) signaling, observed at 14 dpe. After prolonged exposure to 21 dpe, both autophagic and inflammatory pathways were downregulated. qPCR confirmed this time-dependent expression profile for key genes associated with autophagy (sqstm1, map1lc3b, atg4d, atg5, becn1) and immune (il1β, nlrp3, tgfβ, map3k7, tnfa, tnfb, myd88) function. Pharmacological inhibition of autophagy by 3-methyladenine (3-MA) markedly abrogated the activation of NLR and MAPK signaling genes at 14 dpe, confirming a causal regulatory link between autophagy and innate immunity. Collectively, these findings suggest that microplastic exposure triggers a sequential immunotoxic transition in the fish liver. The early induction of autophagy may support subsequent immune activation, which eventually shifts to a broad suppression of immune pathways under sustained stress. This study offers new insight into the dynamic interaction between autophagy and innate immunity during microplastic-induced hepatotoxicity and highlights the potential risk of immunosuppression after long-term microplastic exposure.
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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.
Toxic effects of microplastics on freshwater fish (Channa argus): mechanisms of inflammation, apoptosis, and autophagy
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Freshwater snakehead fish exposed to polystyrene microplastics for four weeks developed inflammation, cell death, and tissue damage in their liver, intestines, kidneys, and gills. The damage worsened with higher microplastic concentrations and involved disruption of the fish's antioxidant defenses and immune system. Since snakehead is a commonly consumed fish in Asia, these findings raise questions about whether microplastics in aquaculture environments could affect the safety of fish as human food.
The Mechanism of Combined Exposure of Polystyrene Microplastics and Cadmium Inducing Hepatic Injury through the Modulation of PI3K/AKT/mTOR-Mediated Autophagy
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Researchers examined liver damage in mice exposed to polystyrene microplastics and cadmium, both alone and in combination, and found that triple exposure to 100-nanometer particles, 1-micrometer particles, and cadmium caused the most severe liver dysfunction. The study suggests that nanoscale microplastics significantly enhance cadmium-induced liver injury through disrupted autophagy via the PI3K/AKT/mTOR signaling pathway.
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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.
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.
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