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Endoplasmic reticulum stress exacerbates microplastics-induced toxicity in animal cells
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Researchers investigated how microplastic exposure affects animal cells through a stress response in a cellular structure called the endoplasmic reticulum. They found that microplastics triggered this stress pathway, which amplified toxic effects including inflammation and cell death. The study suggests that endoplasmic reticulum stress may be an important and previously underappreciated mechanism through which microplastics cause damage to tissues.
Human and animal exposure to microplastics (MPs) contained in food is inevitable because of their widespread existence in the environment. Nevertheless, MPs toxicity studies in ruminants often lack attention. Here, we assessed the cytotoxicity of polystyrene microplastics (PS MPs) on goat mammary epithelial cells (GMECs). Compared to controls, PS MPs treatment significantly reduced cell viability, altered cell morphology and disrupted organelle integrity. Detection of membrane potential and reactive oxygen species (ROS) suggested that PS MPs induced mitochondrial dysfunction and oxidative stress. Further transcriptome analysis also confirmed alterations in these pathways. In addition, several genes related to endoplasmic reticulum (ER) homeostasis were significantly regulated in the transcriptional profile. Subsequent experiments confirmed that PS MPs induce ER stress via the PERK/eIF2α/CHOP pathway, accompanied by intracellular Ca overload. Meanwhile, downstream activation of the Bax/Bcl-2 pathway and caspase cascade released apoptotic signals, which led to apoptosis in GMECs. Interestingly, the addition of PERK inhibitor (ISRIB) attenuated PS MPs-induced ER stress and apoptosis, which suggests that ER stress may exacerbate PS MPs-induced cytotoxicity. This work reveals the impact of MPs on mammalian cytotoxicity, enriches the mechanisms for the toxicity of MPs, and provides insight for further assessment of the risk of MPs in food.
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Researchers found that polystyrene microplastics caused growth problems and bone damage in young rats by triggering stress in a part of the cell called the endoplasmic reticulum. This stress disrupted the normal process by which cartilage turns into bone in growing animals. The findings raise concerns that microplastic exposure during early development could interfere with normal bone growth in children.
Fluorescent visualization of endoplasmic reticulum stress induced by microplastic pollution via surge of intracellular reactive oxygen species
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Researchers used peroxynitrite as a fluorescent probe to visualize how microplastics trigger endoplasmic reticulum (ER) stress inside cells, finding that MP invasion causes a surge in reactive oxygen species that activates ER stress pathways. The study clarified a key molecular mechanism linking microplastic internalization to cellular disease processes.
Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)
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Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.
Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens
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Researchers exposed chickens to polystyrene microplastics for 42 days and found significant lung damage, including tissue inflammation and cell stress responses. The microplastics triggered a chain reaction starting with stress in the endoplasmic reticulum (a cell structure involved in protein processing) that activated inflammatory pathways. While this study focused on poultry, similar inflammatory mechanisms could be relevant to understanding how microplastics affect lungs in other species, including humans.
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