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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.
Microplastics (MPs) seriously pollute and potentially threaten human health. Birds are sentinels of environmental pollutants, which respond quickly to contamination events and reveal current environmental exposure. Therefore, birds are good bioindicators for monitoring environmental pollutants. However, the mechanism of lung injury in birds and the role of the PTEN/PI3K/AKT axis are unknown. In this study, broilers treated with different polystyrene microplastics (PS-MPs) (0, 1, 10, and 100 mg/L) were exposed to drinking water for 6 weeks to analyze the effect of PS-MPs on lung injury of broilers. The results showed that with the increase of PS-MPs concentration, malonaldehyde (MDA) content increased, and catalase (CAT) and glutathione (GSH) activity decreased, further leading to oxidative stress. PS-MPs caused the PI3K/Akt/mTOR pathway to be inhibited by phosphorylation, and autophagy accelerated formation (LC3) and degradation (p62), causing autophagy. In PS-MPs exposed lung tissues, the expression of Bax/Bcl-2 and Caspase family increased, and MAPK signaling pathways (p38, ERK, and JNK) showed an increase in phosphorylation level, thus leading to cell apoptosis. Our research showed that PS-MPs could activate the antioxidant system. The antioxidant system unbalance-regulated Caspase family, and PTEN/PI3K/AKT pathways initiated apoptosis and autophagy, which in turn led to lung tissue damage in chickens. These results are of great significance to the toxicological study of PS-MPs and the protection of the ecosystem.
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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.
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.
Polystyrene microplastics with different sizes induce the apoptosis and necroptosis in liver through the PTEN/PI3K/AKT/autophagy axis
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Mice exposed to polystyrene microplastics of different sizes developed liver damage through two types of cell death: apoptosis and necroptosis. Smaller microplastics caused more severe damage, disrupting a key cell survival pathway called PTEN/PI3K/AKT and impairing the liver's self-cleaning process (autophagy). The study suggests that the smallest microplastic particles may pose the greatest liver health risk because they penetrate cells more readily.
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