0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Gut & Microbiome Human Health Effects Nanoplastics Sign in to save

Maltol attenuates polystyrene nanoplastic-induced enterotoxicity by promoting AMPK/mTOR/TFEB-mediated autophagy and modulating gut microbiota

Environmental Pollution 2023 43 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ming-hui Jin, Junnan Hu, Ming Zhang, Zhaojie Meng, Guo‐Ping Shi, Zi Wang, Wei Li

Summary

Researchers found that maltol, a natural food flavoring compound, can protect against intestinal damage caused by polystyrene nanoplastics in mice. Maltol worked by activating cellular cleanup processes (autophagy) and restoring the balance of gut bacteria disrupted by nanoplastic exposure. The study suggests that dietary compounds like maltol could potentially help mitigate some of the gut health effects associated with nanoplastic ingestion.

Polymers
Models

The production and application of nanoplastics has been increased during decades, and the enterotoxicity caused by their bioaccumulation has attracted vast attention. Maltol was proved to exert a protective effect on gut damage induced by carbon tetrachloride and cisplatin, indicating its confrontation with nanoplastics-induced intestinal toxicity. To explore the ameliorative effects of maltol on polystyrene nanoplastics (PS)-mediated enterotoxicity and the underlying mechanism, the mice were exposed to PS (100 mg/kg), combining with or without the treatment of maltol treatment at 50 and 100 mg/kg. We found PS exposure caused intestinal barrier damage and enterocyte apoptosis, while lysosomal dysfunction and autophagic substrate degradation arrest in enterocytes of mice were also observed. In addition, PS exacerbated the disturbance of the intestinal microbial community, affected the abundance of lysosome and apoptosis-related bacterial genes, and decreased the number of known short-chain fatty acid (SCFA) producing bacteria. However, those alterations were improved by the maltol treatment. Maltol also protected the human intestinal Caco-2 cells from PS-induce damages. Mechanistic studies showed maltol promoted TFEB nuclear translocation through the AMPK/mTOR signaling pathway to restore lysosomal function and reduce autophagy dependent apoptosis. The findings in the present work might help to elucidate the potential molecular mechanisms of PS-induced enterotoxicity. For the first time to our knowledge, the protective effect of maltol on PS-induced intestinal injury was studied from multiple perspectives, which provided a potential therapeutic approach for diseases caused by environmental pollution.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Quercetin intervention mitigates small intestinal damage and immunologic derangement induced by polystyrene nanoplastics: Insights from multi-omics analysis in mice

Researchers found that quercetin, a natural compound found in fruits and vegetables, protected mice from gut damage and immune system disruption caused by polystyrene nanoplastics. The nanoplastics damaged the small intestine and disrupted immune balance, but quercetin reversed much of this harm by restoring healthy gut bacteria and gene activity. This suggests that dietary compounds like quercetin might help counteract some negative health effects of nanoplastic exposure.

Article Tier 2

Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs

Researchers found that polystyrene nanoplastics disrupt the gut lining in mice by altering tiny RNA molecules that control the production of protective proteins in the intestinal barrier. The nanoplastics also caused an imbalance in gut bacteria, creating a chain reaction where damaged gut cells release particles that further weaken the intestinal barrier and change the microbiome.

Article Tier 2

Polystyrene nanoparticles induced mammalian intestine damage caused by blockage of BNIP3/NIX-mediated mitophagy and gut microbiota alteration

Researchers found that polystyrene nanoparticles can damage the intestines of mammals by blocking a cellular cleanup process called mitophagy, which normally removes damaged mitochondria. In both cell cultures and animal models, exposure to these nanoparticles disrupted gut barrier function and altered gut microbiota composition. The study suggests that nanoplastic accumulation in food sources could pose a real risk to digestive health.

Article Tier 2

Lactic acid bacteria reduce polystyrene micro- and nanoplastics-induced toxicity through their bio-binding capacity and gut environment repair ability

Researchers found that lactic acid bacteria, the kind used in yogurt and fermented foods, can reduce the toxic effects of polystyrene micro and nanoplastics in mice. The bacteria worked by physically binding to the plastic particles and by repairing damage to the gut lining and restoring healthy gut bacteria populations. This suggests that probiotics could be a practical way to help protect the digestive system from the harmful effects of microplastic exposure through food and water.

Article Tier 2

Interactions between intestinal microbiota and metabolites in zebrafish larvae exposed to polystyrene nanoplastics: Implications for intestinal health and glycolipid metabolism

Zebrafish larvae exposed to polystyrene nanoplastics suffered intestinal damage, including inflammation, oxidative stress, and disrupted gut bacteria -- with increases in bacteria linked to gut disease. The nanoplastics also altered metabolism related to sugar and fat processing, suggesting that ingesting these tiny particles could harm digestive health and disrupt how the body processes nutrients.

Share this paper