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Polystyrene nanoplastics trigger ferroptosis-dependent liver injury caused by ACSL4 overaccumulation.
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In liver cells and mice, exposure to polystyrene nanoplastics caused liver damage linked to a cell death process called ferroptosis. The plastics disrupted lysosomes, cell structures involved in breaking down materials, leading to buildup of a protein called ACSL4 that drove this damage.
Nanoplastics (NPs) are persistent environmental pollutants that can accumulate in the liver, but the mechanisms of their hepatotoxicity remain poorly understood. Here, using AML12 cells and a mouse model, we investigated how polystyrene nanoplastics (PS-NPs) cause liver injury. Exposure to PS-NPs induced dose-dependent cytotoxicity and ferroptosis, evidenced by elevated Fe²⁺ and reactive oxygen species (ROS) levels, enhanced lipid peroxidation, glutathione peroxidase 4 (GPX4) downregulation, and acyl-CoA synthetase long chain family member 4 (ACSL4) upregulation. PS-NPs exposure increased hepatic pathological injury scores and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in vivo. Treatment with ferrostatin-1 (Fer-1) markedly attenuated these changes. Mechanistically, PS-NPs exposure disrupted lysosomal function, as shown by reduced expression of lysosome-associated membrane proteins and increased lysosomal pH. This lysosomal impairment hindered degradative capacity and led to ACSL4 accumulation. Restoring lysosomal function with NKH477 reduced ACSL4 levels. Together, these findings suggest that PS-NPs promote hepatocyte ferroptosis through lysosomal dysfunction and subsequent ACSL4 accumulation. This study provides new insight into the mechanisms of PS-NPs-induced liver toxicity and highlights potential targets for intervention.
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Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
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Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.
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.
Inert polystyrene nanoplastics-induced liver injury in mice was implicated in intense oxidative stress and inflammation mediated by ferroptosis.
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Scientists injected mice with nanoplastics (tiny plastic particles similar to those found in our food and water) and found they triggered liver damage through a specific type of cell death linked to iron and oxidative stress, along with signs of kidney stress. While this study used direct injection into mice rather than everyday human exposure, it adds to growing evidence that the nanoplastics we're increasingly exposed to through food and packaging could harm multiple organs, not just the gut where they're first absorbed.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
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Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Hepatotoxic mechanisms of functionalized nanopolystyrene: decoding the role of ionic surface groups
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Researchers exposed mice to polystyrene nanoplastics with different surface charges via drinking water, finding that charged particles accumulate in liver sinusoids and induce hepatocyte ferroptosis through an endoplasmic reticulum stress cascade, while neutral particles cause endothelial cell senescence through lysosomal dysfunction.
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