Avermectin (AVM) has been widely used in agriculture and animal husbandry based on its broad spectrum of effective anthelmintic activity and specificity targets. However, AVM induction of cytotoxicity in human liver is largely unknown. In this study, we investigate the cytotoxic effects of AVM on HepG2 cells in vitro. The results revealed that AVM inhibited the viability of HepG2 cells and enhanced apoptosis. Established assays of cytotoxicity were performed to characterize the mechanism of AVM toxicity on HepG2 cells. Typical apoptosis morphological changes were shown in AVM-treatment cells including chromatin condensation and DNA fragmentation. We demonstrated that AVM-induced apoptosis of HepG2 cells were mediated by generated ROS. Moreover, a decrease in mitochondrial membrane potential (MMP) and up-regulating the Bax/Bcl-2 ratio, resulted in a release of cytochrome-c as well as activation of caspase-9/-3. In conclusion, our experimental results show that AVM has a potential threat to human health which may be induce apoptosis of human hepatocyte cells via caspase-dependent mitochondrial pathways.

The overdosage use of pesticide was harmful to the environment and human health, which was mainly caused by the low utilization rate of the pesticide. However, the pesticide microcapsule with sustained-release and stimulating response properties could effectively solve this problem. Preparation of carboxymethyl cellulose grafting dimethyldiallylammonium chloride (CMC-g-PDMDAAC) through grafting polymerization and trapping as well as encapsulation of avermectin (AVM) via electrostatic interactions resulted in the formation of AVM/CMC-g-PDMDAAC microcapsules. The results showed that the particle size was 200~300 nm. The encapsulation efficiency was as high as 72.06%. Furthermore, the remaining rate of encapsulated AVM increased from 50.0 to 81.60% after UV irradiation for 359 min. The microcapsules exhibited significant enzyme and pH stimuli responsiveness. Finally, CMC-g-PDMDAAC had no significant difference effect on the toxicity of AVM, AVM could be found, and DMDAAC featured a synergistic effect on the toxicological effects of AVM. Graphical abstract

Pesticide residue in mushrooms is less known. In this study, the risks of beta-cypermethrin, pyriproxyfen, avermectin, and diflubenzuron in oyster and shiitake mushrooms were evaluated using two different treatments: substrate mixture and surface spraying. Almost all the concentrations of these pesticides at day 90 were higher than 80% of the initial concentrations, while it was less than 45% for all cases within 35 days by spraying. For surface spraying, the residues of beta-cypermethrin were 0.0843–1.22 mg kg⁻¹ in shiitake mushrooms and below 0.005 mg kg⁻¹ in oyster mushrooms; the residues of pyriproxyfen, avermectin, and diflubenzuron were 0.122–4.84, 0.00501–0.111, and 0.0681–1.91 mg kg⁻¹, respectively. The residues of beta-cypermethrin, pyriproxyfen, and diflubenzuron in oyster mushrooms (in shiitake mushrooms) at interval of 0, 3, 5 days (1, 5, 7 days) were below their MRLs in China or Japan. The residue of avermectin in both mushrooms was lower than its limit of detection. These results provide information to safe and proper use of the pesticides in oyster and shiitake mushrooms.

Pesticide residues are an important aspect of environmental pollution. Environmental avermectin residues have produced adverse effects in organisms. Many pesticides exert their toxic effects via the mechanism of autophagy. The purpose of this study was to examine the changes in autophagy levels and in autophagy-related genes, including LC3, Beclin 1, Dynein, ATG5, TORC1, and TORC2, resulting from exposure to subchronic levels of AVM in liver tissue in the king pigeon model. We observed abundant autophagic vacuoles with extensively degraded organelles, autophagosomal vacuoles, secondary lysosomes, and double-membrane structures in the liver. The expression levels of the autophagy-related genes LC3-I, LC3-II, Beclin 1, ATG5, and Dynein were up-regulated; however, TORC1 and TORC2 expression levels were down-regulated. These changes occurred in a concentration-dependent manner after AVM exposure for 30, 60, and 90 days in pigeons. Taken together, these results suggested that AVM increased the autophagic flux and that upregulation of autophagy might be closely related to the hepatotoxicity of AVM in birds.