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

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-κß 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.

Microplastics exposure as an emerging threat to ancient lineage: A contaminant of concern for abnormal bending of amphioxus via neurotoxicity.

Growing inputs of microplastics into marine sediment have increased significantly the needs for assessment of their potential risks to the marine benthos. A knowledge gap remains with regard to the effect of microplastics on benthos, such as cephalochordates. By employing amphioxus as a model benthic chordate, here we show that exposure to microplastics for 96 h at doses of 1 mg/L and 100 mg/L results in evident accumulation of the polyethylene microplastics. The accumulated microplastics are as much as 0.027% of body weight upon high-dose exposure, causing an abnormal body-bending phenotype that limits the locomotion capability of amphioxus. Mechanistic insight reveals that microplastics can bring about histological damages in gill, intestine and hepatic cecum; In-depth assay of relevant biomarkers including superoxide dismutase, catalase, glutathione, pyruvic acid and total cholesterol indicates the occurrence of oxidative damage and metabolic disorder; Further, microplastics exposure depresses the activity of acetylcholinesterase while allowing the level of acetylcholine to rise in muscle, suggesting the emergence of neurotoxicity. These consequences eventually contribute to the muscle dysfunction of amphioxus. This study rationalizes the abnormal response of the vulnerable notochord to microplastics, signifying the dilemma suffered by the ancient lineage under the emerging threat. Given the enrichment of microplastics through marine food chains, this study also raises significant concerns on the impact of microplastics to other marine organisms, and eventually human beings.

Production of monoclonal antibody against EP0 protein of pseudorabies virus and determination of its recognized epitope.

Early protein 0 (EP0) is especially important for modulating PRV gene expression and reactivation from the latent state, but the mechanisms have not been elucidated. In this study, six monoclonal antibodies (MAbs) against EP0 protein of PRV were generated and their characterizations were investigated. Western blot analysis showed all six MAbs could react with immunizing antigen, but only 2B12 and 2C6 could react with native EP0 protein from PRV-infected cells. ELISA additivity tests revealed that at least three epitopes in EP0 were defined by six MAbs. The epitope recognized by MAb 2B12 was further identified in 287-292 aa of EP0 protein using a series of expressed overlapping peptides. These MAbs may provide valuable tools for further research of the functions of EP0 in PRV infection.