Polystyrene nanoplastics exacerbate aflatoxin B1-induced hepatic injuries by modulating the gut−liver axis

• Published in: The Science of the total environment Vol. 935; p. 173285
• Main Authors: Zhang, Kai-Kai, Wan, Jia-Yuan, Chen, Yu-Chuan, Cheng, Chang-Hao, Zhou, He-Qi, Zheng, De-Kai, Lan, Zhi-Xian, You, Qiu-Hong, Sun, Jian
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 20.07.2024
• Subjects: Aflatoxin B1; Aflatoxin B1 - toxicity; Animals; Chemical and Drug Induced Liver Injury; Dysbiosis - chemically induced; Gastrointestinal Microbiome - drug effects; Gut microbiota; Gut−liver axis; Hepatic injuries; Liver - drug effects; Mice; Microplastics - toxicity; Nanoparticles - toxicity; Polystyrene nanoplastics; Polystyrenes - toxicity; Gut microbiota; Aflatoxin B1; Hepatic injuries; Gut−liver axis; Polystyrene nanoplastics
• ISSN: 0048-9697; 1879-1026
• DOI: 10.1016/j.scitotenv.2024.173285

Dietary pollution of Aflatoxin B1 (AFB1) poses a great threat to global food safety, which can result in serious hepatic injuries. Following the widespread use of plastic tableware, co-exposure to microplastics and AFB1 has dramatically increased. However, whether microplastics could exert synergistic effects with AFB1 and amplify its hepatotoxicity, and the underlying mechanisms are still unelucidated. Here, mice were orally exposed to 100 nm polystyrene nanoplastics (NPs) and AFB1 to investigate the influences of NPs on AFB1-induced hepatic injuries. We found that exposure to only NPs or AFB1 resulted in colonic inflammation and the impairment of the intestinal barrier, which was exacerbated by combined exposure to NPs and AFB1. Meanwhile, co-exposure to NPs exacerbated AFB1-induced dysbiosis of gut microbiota and remodeling of the fecal metabolome. Moreover, NPs and AFB1 co-exposure exhibited higher levels of systemic inflammatory factors compared to AFB1 exposure. Additionally, NPs co-exposure further exacerbated AFB1-induced hepatic fibrosis and inflammation, which could be associated with the overactivation of the TLR4/MyD88/NF-κB pathway. Notably, Spearman's correlation analysis revealed that the exacerbation of NPs co-exposure was closely associated with microbial dysbiosis. Furthermore, microbiota from NPs-exposed mice (NPsFMT) partly reproduced the exacerbation of NPs on AFB1-induced systemic and hepatic inflammation, but not fibrosis. In summary, our findings indicate that gut microbiota could be involved in the exacerbation of NPs on AFB1-induced hepatic injuries, highlighting the health risks of NPs. [Display omitted] •NPs aggravated AFB1-induced intestinal barrier impairment and colonic inflammation.•NPs aggravated AFB1-induced gut microbial dysbiosis and reshaped fecal metabolome.•NPs aggravated AFB1-induced hepatic inflammation and fibrosis.•Gut microbiota mediated the exacerbation of NPs on AFB1-induced hepatic inflammation.