Nanoplastics (NPs) are currently everywhere and environmental pollution by NPs is a pressing global problem. Nevertheless, until now, few studies have concentrated on the mechanisms and pathways of cytotoxic effects and immune dysfunction of NPs on soil organisms employing a multidimensional strategy. Hence, earthworm immune cells and immunity protein lysozyme (LZM) were selected as specific receptors to uncover the underlying mechanisms of cytotoxicity, genotoxicity, and immunotoxicity resulting from exposure to polystyrene nanoplastics (PS-NPs), and the binding mechanisms of PS-NPs-LZM interaction. Results on cells indicated that when earthworm immune cells were exposed to high-dose PS-NPs, it caused a notable rise in the release of reactive oxygen species (ROS), resulting in oxidative stress. PS-NPs exposure significantly decreased the cell viability of earthworm immune cells, inducing cytotoxicity through ROS-mediated oxidative stress pathway, and oxidative injury effects, including reduced antioxidant defenses, lipid peroxidation, DNA damage, and protein oxidation. Moreover, PS-NPs stress inhibited the intracellular LZM activity in immune cells, resulting in impaired immune function and immunotoxicity by activating the oxidative stress pathway mediated by ROS. The results from molecular studies revealed that PS-NPs binding destroyed the LZM structure and conformation, including

Tebuconazole has been widely applied over three decades because of its high efficiency, low toxicity, and broad spectrum, and it is still one of the most popular fungicides worldwide. Tebuconazole residues have been frequently detected in environmental samples and food, posing potential hazards for humans. Understanding the toxicity of pesticides is crucial to ensuring human and ecosystem health, but the toxic mechanisms and toxicity of tebuconazole are still unclear. Moreover, pesticides could transform into transformation products (TPs) that may be more persistent and toxic than their parents. Herein, the toxicities of tebuconazole to humans, mammals, aquatic organisms, soil animals, amphibians, soil microorganisms, birds, honeybees, and plants were summa-rized, and its TPs were reviewed. In addition, the toxicity of tebuconazole TPs to aquatic organisms and mam-mals was predicted. Tebuconazole posed potential developmental toxicity, genotoxicity, reproductive toxicity, mutagenicity, hepatotoxicity, neurotoxicity, cardiotoxicity, and nephrotoxicity, which were induced via reactive oxygen species-mediated apoptosis, metabolism and hormone perturbation, DNA damage, and transcriptional abnormalities. In addition, tebuconazole exhibited apparent endocrine-disrupting effects by modulating hormone levels and gene transcription. The toxicity of some TPs was equivalent to and higher than tebuconazole. Therefore, further investigation is necessary into the toxicological mechanisms of tebuconazole and the combined toxicity of a mixture of tebuconazole and its TPs.

Imidacloprid (IMI), a neonicotinoid insecticide, has a wide variety of applications in both agriculture and horticulture. As a result of it massive and repeated use, its traces remained in soil pose severe damage to soil invertebrates, particularly earthworms. Limited information is available regarding the underlying mechanisms of IMI toxicity toward earthworms at the molecular, transcriptional, and cellular levels. Here, Eisenia fetida coelomocytes and key defensive proteins were selected as targeted receptors to explore the toxic mechanisms of oxidative stress-mediated cytotoxicity, genotoxicity, and antioxidant responses induced by IMI stress and the molecular mechanisms underlying the binding of IMI and superoxide dismutase (SOD)/catalase (CAT). Results showed that IMI exposure destroyed the cell membrane integrity of earthworm cells, causing cell damage and cytotoxicity. The intracellular levels of ROS, including center dot O-2(-) and H2O2 were induced by IMI exposure, thereby triggering oxidative stress and damage. Moreover, IMI exposure attenuated the antioxidative stress responses (reduced antioxidant capacity and CAT/SOD activities) and caused deleterious effects (enhanced DNA damage, lipid peroxidation (LPO), and protein carbonylation (PCO)) through ROS-mediated oxidative stress pathway. Aberrant gene expression associated with oxidative stress and defense regulation, including CAT, CRT, MT, SOD, GST, and Hsp70 were induced after IMI exposure. Concentration-dependent conformational and structural alterations of CAT/SOD were observed when IMI binding. Also, direct binding of IMI resulted in significant inhibition of CAT/SOD activities in vitro. Molecular simulation showed that IMI preferred to bind to CAT active center through its direct binding with the key residue Tyr 357, while IMI bound more easily to the connecting cavity of two subunits away from SOD active center. In addition, hydrogen bonds and hydrophobic force are the main driving force of IMI binding with CAT/SOD. These findings have implications for comprehensive evaluation of IMI toxicity to soil eco-safety and offer novel strategies to elucidate the toxic mechanisms and pathways of IMI stress.