Sight of Aged Microplastics Adsorbing Heavy Metal Exacerbated Intestinal Injury: A Mechanistic Study of Autophagy-Mediated Toxicity Response

微塑料 毒性 金属毒性 自噬 重金属 环境化学 化学 生物 环境卫生 医学 生物化学 内科学 细胞凋亡
作者
Weike Shaoyong,Sun Lu,Yujie Gan,Hongli Jin,Wusu Wang,Lin Yin,Yizhen Wang,Mingliang Jin
出处
期刊:ACS Nano [American Chemical Society]
卷期号:18 (42): 28849-28865 被引量:48
标识
DOI:10.1021/acsnano.4c08737
摘要

Contaminant-bearing polystyrene microplastics (PSMPs) may exert significantly different toxicity profiles from their contaminant-free counterparts, with the role of PSMPs in promoting contaminant uptake being recognized. However, studies investigating the environmentally relevant exposure and toxic mechanisms of aged PSMPs binding to Cr are limited. Here, we show that loading of chromium (Cr) markedly alters the physicochemical properties and toxicological profiles of aged PSMPs. Specifically, Cr-bearing aged PSMPs induced severe body weight loss, oxidative stress (OS), autophagy, intestinal barrier injury, inflammation-pyroptosis response, and enteropathogen invasion in mice. Mechanistic investigations revealed that PSMPs@Cr exacerbated the OS, resulting in intestinal barrier damage and inflammation-pyroptosis response via overactivated Notch signaling and autophagy/cathepsin B/IL-1β pathway, respectively, which ultimately elevated mortality related to bacterial pathogen infection. In vitro experiments confirmed that autophagy-mediated reactive oxygen species (ROS) overproduction resulted in severe pyroptosis and impaired intestinal stem cells differentiation alongside the overactivation of Notch signaling in PSMPs@Cr-exposed organoids. Overall, our findings provide an insight into autophagy-modulated ROS overproduction within the acidic environment of autophagosomes, accelerating the release of free Cr from PSMPs@Cr and inducing secondary OS, revealing that PSMPs@Cr is a stable hazard material that induces intestinal injury. These findings provided a potential therapeutic target for environmental MPs pollution caused intestinal disease in patients.
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