title: Avermectin induced liver injury in pigeon: mechanisms of apoptosis and oxidative stress.
abstract: Extensive use of avermectin (AVM) can result in environment pollution, and it is important to evaluate the potential impact this antibiotic has on ecological systems. Few published literatures have discussed the liver injury mechanisms induced by AVM on birds. In this study, pigeons were exposed to feed containing AVM (0, 20, 40 and 60 mg/kg diet) for 30, 60, 90 days respectively. The results showed that AVM increased the number of apoptosis and the expression level of caspase-3, 8, fas mRNA in the liver of pigeons. Ultrastructural alterations, including mitochondrial damage and chromatin aggregation, become severe with increase exposure dose. Exposure to AVM induced significant changes in antioxidant enzyme {superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)} activities and malondialdehyde (MDA) content, augmented protein carbonyl (PCO) content and DNA-protein crosslink (DPC) coefficient, in a concentration-dependent manner in the liver of pigeons. Our results show that AVM has toxic effect in pigeon liver, and the mechanism of injury caused by AVM is closely related to apoptosis and oxidative stress.
authors.affiliation: Department of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Zhu
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Ci
authors.initials: C
authors.lastname: Liu
authors.forename: Jian-Ping
authors.initials: JP
authors.lastname: Qu
authors.forename: Ya-Hong
authors.initials: YH
authors.lastname: Min
authors.forename: Shi-Wen
authors.initials: SW
authors.lastname: Xu
authors.forename: Shu
authors.initials: S
authors.lastname: Li
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000633:toxicity*; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D010856:Columbidae / Q000378:metabolism*; D004249:DNA Damage; D053222:Fas Ligand Protein / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007559:Ivermectin / Q000031:analogs & derivatives* / Q000633:toxicity; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008930:Mitochondria, Liver / Q000187:drug effects / Q000648:ultrastructure; D018384:Oxidative Stress; D050050:Protein Carbonylation; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D000975:Antioxidants; D053222:Fas Ligand Protein; D008315:Malondialdehyde; D007559:Ivermectin; C019264:avermectin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D053148:Caspase 3; D053181:Caspase 8
keywords: 2,4-dinitrophenylhydrazine; AVM; Apoptosis; Avermectin; DNA–protein crosslinks; DNPH; DPC; EDTA; FasL; GSH-Px; Liver; MDA; Oxidative stress; PCO; Pigeon; ROS; SOD; ethylenediamine tetraacetic acid; fas ligand; glutathione peroxidase; malondialdehyde; protein carbonyl; reactive oxygen species; superoxide dismutase