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Polystyrene microplastics exacerbate mitophagy through mitochondrial dysfunction in the duck lung
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Ducks fed polystyrene microplastics developed lung inflammation and damage through a process where the plastics disrupted the energy-producing mitochondria in lung cells, triggering excessive cell self-destruction. The study confirmed these findings in both live ducks and lab-grown lung cells, showing that the microplastics activated inflammatory pathways and disrupted normal energy metabolism. Since ducks are widely consumed as food, the research highlights how microplastics can damage poultry lung health and provides insights into how inhaled or ingested microplastics might similarly harm human lungs.
Microplastics (MPs) are widespread environmental pollutants that can enter the human body through the food chain, potentially leading to lung damage. However, the underlying mechanisms responsible for this damage remain unclear. Ducks, a commonly consumed poultry species in China, are particularly susceptible to MPs exposure due to their farming environment. In this study, Shaoxing ducklings were administered two distinct concentrations of polystyrene microplastics (PS-MPs) (1 mg/L and 100 mg/L) via oral route, alongside a control group, over a period of four weeks to establish an in vivo model for evaluating the effects of microplastic exposure in ducks. Simultaneously, rat type II alveolar epithelial (RLE-6TN) cells were exposed to different concentrations of PS-MPs (0, 10, 100, and 500 µg/mL) for 48 h, thereby constructing an in vitro exposure model. Our results showed that PS-MPs caused pathological damage, inflammatory cell infiltration, and activation of the LPS/TLR4 inflammatory pathway in the lung. Further analysis revealed that PS-MPs disrupted the tricarboxylic acid (TCA) cycle and inhibited oxidative phosphorylation. Mechanistic investigation demonstrated that PS-MPs induced mitochondrial dysfunction and consequent excessive mitophagy. This study investigates the mechanisms by which PS-MPs contribute to mitochondrial dysfunction and mitophagy, potentially exacerbating lung inflammation, offering valuable insights for mitigating the toxic effects of PS-MPs on human and animal health.
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Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
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Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
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.
New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
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Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
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Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR
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Researchers exposed broiler chickens to different concentrations of polystyrene microplastics and examined the effects on their lungs. They found that microplastics triggered cell death and autophagy in lung tissue through a specific signaling pathway involving PTEN, PI3K, AKT, and mTOR. The study provides evidence that inhaled microplastics can cause significant lung damage in birds, which serve as useful bioindicators for monitoring environmental pollution.
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