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Polystyrene Microplastics Induce Sustained Cardiovascular Redox Imbalance and Alter Mitochondrial Quality Control
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Rats fed microplastics for 70 days showed lingering heart problems even after 35 days without exposure—their heart cells had damaged "power plants" (mitochondria), more harmful oxidative stress, and disrupted cellular cleanup processes, all at doses too low to cause obvious symptoms or weight changes. This matters because it suggests microplastic exposure may cause hidden, long-lasting heart damage that doesn't show up in typical checkups, and simply avoiding microplastics afterward may not be enough to reverse the harm.
Microplastic exposure is an emerging environmental risk factor for cardiovascular health; however, whether cardiovascular alterations can be detected after exposure cessation remains unclear. This study investigated subclinical cardiovascular alterations following repeated oral exposure to polystyrene microplastics (PSMPs), with particular emphasis on redox imbalance and mitochondrial function in delayed cardiovascular alterations. Male Sprague-Dawley rats were administered 0.5 μm PSMPs via oral gavage at varying dosages of 5 or 20 mg/kg every 5 days for 70 days, followed by a 35-day exposure-free period. Repeated exposure to PSMPs did not affect body or organ weights but altered cardiac serum biochemical markers. Cardiac tissue exhibited elevated NADPH oxidase 4 (NOX4) expression and decreased superoxide dismutase 1 (SOD1), SOD2, and catalase (CAT) activities, whereas malondialdehyde (MDA) levels remained unchanged, indicating a state of chronic, low-level oxidative stress. Mitochondrial respiratory chain activities, including nicotinamide adenine dinucleotide cytochrome c reductase (NCCR) and succinate cytochrome c reductase (SCCR), were significantly reduced. Ultrastructural analysis revealed mitochondrial swelling and cristae disruption. In parallel, mitochondrial biogenesis-related proteins, including peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1), and mitochondrial transcription factor A (TFAM), were downregulated, while mitophagy markers, including PTEN-induced kinase 1 (PINK1), Parkin RBR E3 ubiquitin protein ligase (Parkin), microtubule-associated protein 1 light chain 3 (LC3), and sequestosome 1 (p62), were upregulated. Notably, most significant alterations were primarily observed in the high-dose group. Furthermore, the aorta showed increased oxidative stress markers without overt structural remodeling. These findings suggest that repeated exposure to PSMP is associated with subclinical cardiac redox–mitochondrial dysregulation, potentially involving redox imbalance, impaired mitochondrial respiratory chain activity, reduced mitochondrial biogenesis, and altered mitochondrial quality-control markers.
More Papers Like This
Polystyrene Nanoplastics Induce Early Mitochondrial Dysfunction in H9c2 Cardiomyoblasts Without Substantial Cell Damage
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Scientists exposed heart muscle cells to nanoplastics (tiny plastic particles similar to those found in human blood and heart tissue) and found that even without killing the cells or causing obvious damage, the plastics quietly disrupted the cells' mitochondria — the "power plants" that generate energy. This means the heart cells' ability to produce extra energy during stress or exertion may be weakened, even though everything looks normal on the surface. While this was a lab study on cells (not people), it raises concern that everyday plastic exposure could be subtly straining our hearts' energy reserves over time.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
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Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
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Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
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.
Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
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Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
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