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Benzo [a] pyrene-loaded aged polystyrene microplastics promote colonic barrier injury via oxidative stress-mediated notch signalling

Journal of Hazardous Materials 2023 53 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Weike Shaoyong, Hongli Jin, Xiao Jiang, Bocheng Xu, Yalin Liu, Yizhen Wang, Mingliang Jin

Summary

Researchers found that aged polystyrene microplastics loaded with benzo[a]pyrene, a common environmental carcinogen, caused significantly more damage to the colon lining in mice than clean microplastics. The contaminated particles triggered oxidative stress, inflammation, and disrupted the protective barrier of the intestine through a specific cell signaling pathway. This suggests that real-world microplastics, which commonly carry absorbed toxic chemicals, may be more harmful to gut health than pristine lab particles.

Polymers
Models

The adsorption of toxic substances on polystyrene microplastics (PSMPs) can modify their biological toxicity and exacerbate the threat to human health. The effects of benzo [a] pyrene (B (a) P)-loaded aged PSMPs on colonic barrier integrity remains unclear. Here, we showed that binding environmentally relevant concentrations of B (a) P alteredl̥ the physicochemical features and markedly enhanced the toxicity of PSMPs. Compared to pristine PSMP, PSMP@B (a) P promoted colonic barrier degradation, body weight loss, colon length shortening, oxidative stress (OS), autophagy, inflammation, and bacterial translocation. Microplastic (MP) exposure induced injury to the colon barrier, including tight junction (TJ) and mucosal barriers, via overactivation of the Notch signalling pathway under increased OS in mice and intestinal organoids. Notably, PSMP@B (a) P exposure exacerbated damage to TJ and the mucosal barrier via the overproduction of reactive oxygen species (ROS), which could be related to the release of B (a) P from PSMP@B (a) P induced by the acidic environment of autophagosomes, which in turn exert synergistic toxic effects with PSMPs. Our study elucidates some of the potential molecular mechanisms by which B (a) P enhances PSMP-related intestinal toxicity, which provides a potential therapeutic approach for diseases caused by PSMP@B (a)P and PSMP pollution.

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