Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR

Abstract

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.

Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells

“…Studies have shown that MPs increase intracellular ROS in human placental cells, which can induce DNA damage and lead to cell cycle arrest in the G1 or G2 phase, autophagy, and apoptosis. 30,31 Most studies concluded that MPs cause cell cycle arrest in the G0/G1 phase, but in our study, G2/M cell cycle arrest. Cell cycle arrest in G2/M and its subsequent downstream signaling are hitherto unrecognized therapeutic targets to block the accelerated progression of renal disease.…”

“…Previous studies have focused on MPs to inhibit cell growth and lead to cycle arrest. Studies have shown that MPs increase intracellular ROS in human placental cells, which can induce DNA damage and lead to cell cycle arrest in the G1 or G2 phase, autophagy, and apoptosis 30,31 . Most studies concluded that MPs cause cell cycle arrest in the G0/G1 phase, but in our study, G2/M cell cycle arrest.…”

Preventive Effects of Apple Polyphenol Extract on High-Fat-Diet-Induced Hepatic Steatosis Are Related to the Regulation of Hepatic Lipid Metabolism, Autophagy, and Gut Microbiota in Aged Mice

“…The enhanced expression of P62 (although not significant) in the HFD group of aged mice suggested the potential inhibition of autophagy, and there was a tendency toward a reduction of P62 expression after APE intervention, which may favor the activation of autophagy. Since ATG5 helps LC3 attach lipids to form autophagosomes, 37 the enhanced expression of ATG5 in HFD-fed aged mice after APE intervention confirmed that APE could exert a protective effect by enhancing autophagy levels in the liver of aged mice.…”

“…The autophagy marker protein LC3 targets the autophagic membrane and participates in autophagosome formation . The P62 protein is an essential selective autophagy junction protein, which is a receptor involved in ubiquitin scavenging .…”

“…The autophagy marker protein LC3 targets the autophagic membrane and participates in autophagosome formation. 37 The P62 protein is an essential selective autophagy junction protein, which is a receptor involved in ubiquitin scavenging. 38 The inhibition of autophagy or a decrease in autophagic flux leads to the accumulation of P62, and the degradation of P62 is a biomarker of autophagic activity.…”