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The mediating role of ferroptosis and mitochondrial dynamics disorder in the aggravation of cardiac injury by polystyrene microplastics
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Researchers investigated how polystyrene microplastics worsen heart injury in mice, particularly when combined with the chemotherapy drug doxorubicin. The study found that microplastics aggravated cardiac damage through ferroptosis and mitochondrial dysfunction pathways, and that two protective compounds, Ferrostatin-1 and luteolin, showed potential in mitigating these harmful effects on heart tissue.
BACKGROUND: Polystyrene microplastics (PS-MPs) represent a major environmental contaminant, capable of building up in various organisms, including animals and plants. They can increase through the food chain, ultimately threatening human health. Recent research has indicated a possible association between exposure to PS-MPs in the environment and heart damage; nevertheless, the specific mechanisms behind this connection are not yet fully understood. OBJECTIVES: This study aimed to investigate the toxic effects of PS-MPs exposure on cardiac health. We specifically elucidated the underlying mechanisms through which PS-MPs exacerbate doxorubicin hydrochloride (DOX)-induced cardiac injury, emphasizing oxidative stress, ferroptosis, and dysregulation of mitochondrial dynamics. Furthermore, we examined the protective effects of two antagonists: Ferrostatin-1 (Fer-1) and luteolin (Lut), against PS-MPs-induced cardiac injury. METHODS: C57BL/6 mice were categorized into eight distinct groups: the blank control group (saline), the PS-MPs exposure group (PS-MPs), the DOX modeling group (DOX), the combined exposure group of PS-MPs and DOX (PS-MPs+DOX), and the treatment groups with Fer-1 and Lut (PS-MPs+Fer-1, PS-MPs+Lut, PS-MPs+DOX+Fer-1, PS-MPs+DOX+Lut). The entire experimental duration spanned five weeks. We evaluated the effects of PS-MPs and DOX on cardiac function using electrocardiography and assessed their impact on cardiac injury through histopathological analysis of the heart. Concurrently, we examined the effects of PS-MPs and DOX on mitochondrial structure via mitochondrial electron microscopy. Furthermore, we analyzed the heart organ coefficient, myocardial injury markers (CK-MB, CTnT), oxidative stress biomarkers (ROS, MDA, GSH, 4-HNE, Nrf2), ferroptosis-related markers (Fe, GPX4, SLC7A11), mitochondrial damage markers (ATP, Complex III, Complex V), mitochondrial dynamics-related markers (OPA1, MNF2, DRP1), as well as serum metabolomics. RESULTS: Our findings reveal that exposure to PS-MPs exhibits significant cardiotoxic effects, influencing heart rate changes in mice and leading to abnormal in oxidative stress levels and ferroptosis-related proteins within myocardial tissue. Concurrently, exposure to PS-MPs leads to changes in mitochondrial structure and dynamics, further exacerbating oxidative stress and ferroptosis. Ultimately, PS-MPs aggravate DOX-induced cardiac injury. However, Fer-1 and Lut have a good improvement effect on the above situation. Furthermore, metabolomic analyses suggest that pathways and metabolites involved in cAMP signaling, the TCA cycle, tryptophan metabolism, and the metabolism of xenobiotics by cytochrome P450 may also play significant roles. CONCLUSION: PS-MPs exposure can further exacerbate DOX-induced cardiac injury in mice, a process characterized by oxidative damage, activation of the ferroptosis pathway, and alterations in mitochondrial dynamics. Furthermore, luteolin, a naturally occurring active compound, plays a significant role in ameliorating this process.
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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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