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Potential Effects of Orally Ingesting Polyethylene Terephthalate Microplastics on the Mouse Heart
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This study found that mice fed PET microplastics (the type of plastic used in water bottles and food containers) developed heart damage, including broken muscle fibers, significant scarring, and cell death in heart tissue. The damage was driven by a buildup of harmful oxygen molecules (oxidative stress) that overwhelmed the heart's natural defenses. These findings raise concern about the potential cardiovascular effects of PET microplastics that humans commonly encounter in food and drink packaging.
Polyethylene terephthalate microplastics (PET MPs) are widespread in natural environment, and can enter organisms and accumulate in the body, but its toxicity has not been well studied. Therefore, in order to investigate the toxic effects of PET microplastics on mammals, this study investigated the toxic effects of PET MPs on ICR mice and H9C2 cells by different treatment groups. The results indicated the cardiac tissue of mice in the PET-H (50 µg/mL) group showed significant capillary congestion, myocardial fiber breakage, and even significant fibrosis compared to the PET-C (control) group (P < 0.01). Results of the TUNEL assay demonstrated significant apoptosis in myocardial tissue in the PET-H and PET-M (5 µg/mL) groups (P < 0.01). Meanwhile, Western blotting showed increased expression of the apoptosis-related protein Bax and decreased expression of PARP, caspase-3, and Bcl-2 proteins in both myocardial tissues and H9C2 cells. In addition, flow cytometry confirmed that PET MPs decreased the mitochondrial membrane potential and apoptosis in H9C2 cells; however, this trend was reversed by N-acetylcysteamine application. Moreover, PET MP treatment induced the accumulation of reactive oxygen species (ROS) in H9C2 cells, while the MDA level in the myocardial tissue was elevated, and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were decreased (P < 0.01), indicating a change in the redox environment. In conclusion, PET MPs promoted cardiomyocyte apoptosis by inducing oxidative stress and activating mitochondria-mediated apoptotic processes, ultimately leading to myocardial fibrosis. This study provides ideas for the prevention of PET MP toxicity and promotes thinking about enhancing plastic pollution control.
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Potential Impact Microplastic Polyethylene Terephthalate on Mice
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Researchers studied how polyethylene terephthalate (PET) microplastics affect mice when ingested, tracking where the particles end up in the body. They found that microplastics accumulated in various organs and caused measurable biological effects. The study adds to growing evidence that common plastic types found in food packaging may pose health risks when consumed.
PET-microplastics trigger endothelial glycocalyx loss via ER stress and ROS unleashing IL-1β-driven SMC switching and early aortic structural impairment
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Scientists found that tiny plastic particles from bottles and food packaging can damage blood vessels when consumed regularly. In lab rats, these microplastics caused harmful changes to the cells lining arteries, which could lead to heart disease over time. This research suggests that plastic pollution may pose a direct threat to our cardiovascular health, though more studies are needed to confirm the effects in humans.
Acute Toxicity Assessment of Orally Administered Microplastic Particles in Adult Male Wistar Rats
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Researchers gave adult male rats a single oral dose of microplastics made from PET water bottles and found that even this one-time exposure altered markers of liver, heart, and kidney function. Higher doses also reduced food intake and increased signs of oxidative stress, which is cell damage caused by harmful molecules. This study suggests that even brief microplastic exposure could trigger early changes in organ function, raising questions about the cumulative effect of daily human exposure through food and water.
Organ-specific accumulation and toxicity analysis of orally administered polyethylene terephthalate microplastics
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When mice were fed tiny PET plastic particles (the kind found in water bottles and food containers), the particles accumulated mainly in the lungs and caused inflammatory damage at higher doses. The study found that male mice were more sensitive than females, and the results highlight that microplastics swallowed through food and drink can travel to and harm organs beyond the digestive system.
Low-dose of polystyrene microplastics induce cardiotoxicity in mice and human-originated cardiac organoids
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Researchers found that even low doses of polystyrene microplastics can damage heart tissue in both mice and lab-grown human heart organoids. The microplastics triggered oxidative stress and disrupted energy production in heart cells, leading to inflammation and cell death. This is one of the first studies to show heart-specific toxicity from microplastics at doses meant to reflect realistic human exposure levels.
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