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Activation of gut metabolite ACSL4/LPCAT3 by microplastics in drinking water mediates ferroptosis via gut–kidney axis
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This study found that polystyrene microplastics carrying the pollutant benzo[a]pyrene caused kidney damage in mice by triggering a type of cell death called ferroptosis through disrupted fat metabolism. The damage occurred through a gut-kidney pathway, where the pollutant-laden microplastics first affected intestinal cells before impacting the kidneys. These findings reveal how microplastics in drinking water could act as carriers for other toxins, amplifying harm to the kidneys.
The environmental pollutant Benzo[a]pyrene (BaP) is commonly found in the environment, with microplastics (MPs) acting as the primary carriers of BaP into living organisms, increasing its availability in the body. However, the specific pathways and mechanisms through which MPs carrying pollutants cause kidney damage are not fully understood. This study aimed to investigate the routes and mechanisms of kidney injury in mice to low concentrations of both MPs and BaP. The combination of polystyrene (PS) and BaP disrupted lipid metabolism in the kidneys, leading to a form of cell death known as ferroptosis. However, this effect was not observed in HK-2 cells in vitro, indicating a cell-specific response. Interestingly, in HIEC-6 cells, both PS and BaP directly induced ferroptosis. These findings confirm that exposure to both PS and BaP can disrupt metabolic homeostasis in the kidneys, contributing to kidney dysfunction and cell death.
More Papers Like This
Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
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Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
The threat of microplastics to human kidney health: Mechanisms of nephrotoxicity and future research directions
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This review examines the growing evidence that microplastics can reach and damage human kidneys, where they were first detected in 2023. Short-term exposure triggers oxidative stress and inflammation, while long-term exposure may lead to kidney scarring through a process called ferroptosis, a type of cell death linked to iron buildup. The authors propose that microplastics may also activate the immune system in kidneys through a gut-kidney connection, highlighting that kidney health is an important but overlooked concern in microplastic research.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
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This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics
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Mice exposed to microplastics showed damaged blood vessels, worse cholesterol levels, and a type of cell death called ferroptosis (basically cells dying from oxidative damage). A drug that blocked this cell death reduced the vessel damage, hinting that microplastics may harm heart and blood vessel health, though this was shown in mice, not yet confirmed in humans.
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