Microplastics (MPs) are important carriers of various toxic metals and can alter their toxicity pattern in agricultural soil, leading to combined pollution, therefore posing new challenges to soil pollution management and environmental risk assessment. In this study, we observed the internalization of MPs in plants and conducted incubation experiments to evaluated the effects of arsenate (As(V)) alone and in combination with polystyrene (PS) MPs on wheat seedlings (Triticum aestivum L.). Under As(V) alone and combined with PS-MP exposure, dosedependent toxicity in terms of root and stem elongation and biomass accumulation was observed. Compared with As(V) alone, the presence of PS-MPs reduced the accumulation of As in wheat roots by 11.43-58.91%, but PSMPs intensified the transport of As to the aboveground parts of wheat, increasing As accumulation in wheat stems by 27.77-1011.54%. This causes more serious mechanical damage and oxidative stress to plant cells, increasing the accumulation of reactive oxygen species and lipid peroxidation in wheat roots and upregulating the activities of antioxidant enzymes such as superoxide dismutase (SOD) and peroxidase (POD). In addition, the co-exposure of As(V) and PS-MPs disrupts the photosynthetic system of wheat leaves and the secretion activities of roots. Therefore, the combination of As(V) and PS-MPs caused greater damage to wheat growth. Our findings contribute to a more comprehensive assessment of the combined toxicity of MPs and heavy metal to crops.

Microplastics' (MPs) ability to sorb and transport polychlorinated biphenyls (PCBs) in soil ecosystems warrants significant attention. Although organisms mainly encounter pollutants through the gut, the combined pollution impact of MPs and PCBs on soil fauna gut toxicity remains incompletely understood. Consequently, this study examined the gut toxicity of polystyrene MPs (PS-MPs) and PCB126 on Eisenia fetida, emphasizing the links between gut bacteria and bacterial translocation instigated by gut barrier impairment. Our findings underscored that E. fetida could ingest PS-MPs, which mitigated the PCB126 accumulation in E. fetida by 9.43 %. Exposure to PCB126 inhibited the expression of gut tight junction (TJ) protein genes. Although the presence of PS-MPs attenuated this suppression, it didn't alleviate gut barrier damage and bacterial translocation in the co-exposure group. This group demonstrated a significantly increased level of gut bacterial load (BLT, ANOVA, p = 0.005 vs control group) and lipopolysaccharide-binding protein (LBP, ANOVA, all p < 0.001 vs control, PCB, and PS groups), both of which displayed significant positive correlations with antibacterial defense. Furthermore, exposure to PS-MPs and PCB126, particularly within the co-exposure group, results in a marked decline in the dispersal ability of gut bacteria. This leads to dysbiosis (Adonis, R-2 = 0.294, p = 0.001), with remarkable signature taxa such as Janthinobacterium, Microbacterium and Pseudomonas, being implicated in gut barrier dysfunction. This research illuminates the mechanism of gut toxicity induced by PS-MPs and PCB126 combined pollution in earthworms, providing novel insights for the ecological risk assessment of soil.