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Exposure to nanoplastics impairs collective contractility of neonatal cardiomyocytes under electrical synchronization
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Researchers studied how nanoplastics affect the contraction of neonatal rat heart cells in the lab. They found that positively charged nanoplastics accumulated on cell membranes and entered cells, leading to reduced calcium levels, disrupted electrical activity, mitochondrial damage, and increased reactive oxygen species, ultimately impairing the heart cells' ability to contract.
Nanoplastics are global pollutants that have been increasingly released into the environment following the degradation process of industrial and consumer products. These tiny particles have been reported to adversely affect various organs in the body, including the heart. Since it is probable that the less-developed hearts of newborn offspring are more vulnerable to nanoplastic insult during the infant feeding compared with mature hearts of adults, the acute effects of nanoplastics on the collective contractility of neonatal cardiomyocytes are to be elucidated. Here, we traced the aggregation of nanoplastics on the cell membrane and their internalization into the cytosol of neonatal rat ventricular myocytes (NRVMs) for 60 min in the presence of electrical pulses to synchronize the cardiac contraction in vitro. The time-coursed linkage of collective contraction forces, intracellular Ca concentrations, mitochondrial membrane potentials, extracellular field potentials, and reactive oxygen species levels enabled us to build up the sequence of the cellular events associated with the detrimental effects of nanoplastics with positive surface charges on the immature cardiomyocytes. A significant decrease in intracellular Ca levels and electrophysiological activities of NRVMs resulted in the reduction of contraction forces in the early phase (0-15 min). The further reduction of contraction force in the late phase (30-60 min) was attributed to remarkable decreases in mitochondrial membrane potentials and cellular metabolism. Our multifaceted assessments on the effect of positively surface charged nanoplastics on NRVM may offer better understanding of substantial risks of ever-increasing nanoplastic pollution in the hearts of human infants or adults.
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Nanoplastics induces arrhythmia in human stem-cells derived cardiomyocytes
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Researchers exposed human cardiomyocytes derived from stem cells to nanoplastic particles and observed dose-dependent uptake, oxidative stress, and arrhythmias developing by day seven. Complementary experiments in mice revealed that nanoplastics disrupted RNA processing and protein folding in heart tissue, leading to cellular stress and impaired electrical signaling. The study provides evidence that nanoplastic exposure may pose direct risks to heart rhythm and function.
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.
Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes
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Researchers exposed human heart cells grown from stem cells to very low doses of polystyrene micro- and nanoplastics over an extended period and found that the particles reduced the cells' ability to contract and disrupted their electrical signaling. The smaller nanoplastics (50 nm) caused more severe damage than the larger microplastics (1 micrometer), including increased cell death and calcium handling problems. This study provides direct evidence that even low-level microplastic exposure could harm human heart function.
PVC nanoplastics impair cardiac function via lysosomal and mitochondrial dysfunction
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Researchers found that PVC nanoplastics damaged heart cells by disrupting two critical cellular structures: lysosomes (the cell's recycling system) and mitochondria (the cell's energy producers). The nanoplastics caused lysosomes to become leaky and mitochondria to malfunction, leading to heart cell injury and impaired cardiac function. This study is concerning because PVC is one of the most common plastics, and the findings suggest that nanoplastic exposure could contribute to heart disease.
Nanoplastics induces Arrhythmia in Human Stem-cells derived Cardiomyocytes
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Exposing human embryonic stem cell-derived heart muscle cells to nanoplastics for up to seven days caused dose-dependent oxidative stress, increased cell death, and — by day seven — abnormal electrical activity consistent with cardiac arrhythmia. These findings provide the first direct evidence using human heart cells that nanoplastic accumulation can disrupt cardiac function, raising important questions about long-term cardiovascular risks from plastic particle exposure in people.
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