Microplastic-contaminated antibiotics as an emerging threat to mammalian liver: enhanced oxidative and inflammatory damages.

Abstract

Poor management and disposal of plastic materials and the accumulation of microplatics in the environment and foods are an issue of increasing public concern. The current understanding of the implications of microplastics for human health has been limited to the bioeffect of individual exposure. In the bigger view of microplastic contamination, however, toxic compounds, including antibiotics, harbored on active microplastics can be collectively transported through food chains, raising questions about the effect of their combined exposure on human health. By employing a mouse model for human physiology, we discovered that a concurrent exposure to the major types of antibiotics and microplastics, namely sulfamethoxazole (SMZ) and polystyrene microplastics, respectively, would result in evident accumulation in detoxification organs; specifically, liver could amass 41.70 μg kg-1 of SMZ, while 3.83% of microplastics was accumulated in the kidney. Insights into the occurrence of liver histopathological changes (e.g., amyloidosis and necrocytosis) revealed that compared with the individual treatment of SMZ, treatment by microplastic-contaminated SMZ elicited increases in the levels of malonaldehyde and NF-κβ by 174% and 104%, respectively; while the activities of antioxidases investigated were depressed by up to 22% upon co-exposure. It is suggested that SMZ enriched on active microplastic surfaces causes enhanced hepatic damage. Profiling of the gene expression clarified the correlation of the exacerbated oxidative and inflammatory damages in the liver with the overexpression of Nrf2 to dysregulate the Keap1-Nrf2 pathway. This study acts as a reminder about the complexity of contamination and raises awareness of health issues that microplastics could cause public health through liver diseases.