PUBLICATION

Short-term developmental toxicity and potential mechanisms of the herbicide metamifop to zebrafish (Danio rerio) embryos

Authors
Zhao, F., Li, H., Cao, F., Chen, X., Liang, Y., Qiu, L.
ID
ZDB-PUB-190902-18
Date
2019
Source
Chemosphere   236: 124590 (Journal)
Registered Authors
Keywords
Acute toxicity, Cell apoptosis, Immune responses, Metamifop, Oxidative stress, Zebrafish
MeSH Terms
  • Anilides/toxicity*
  • Animals
  • Apoptosis/drug effects
  • Benzoxazoles/toxicity*
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental/genetics
  • Herbicides/metabolism
  • Immunity, Innate/genetics
  • Larva/drug effects
  • Larva/metabolism
  • Oxidative Stress/drug effects
  • Oxidative Stress/genetics
  • Reactive Oxygen Species/metabolism
  • Water Pollutants, Chemical/toxicity
  • Zebrafish/embryology
  • Zebrafish/growth & development
  • Zebrafish/metabolism*
PubMed
31470984 Full text @ Chemosphere
Abstract
Metamifop is a novel aryloxyphenoxy propionate (AOPP) herbicide that is widely applied in paddy fields, which will inevitably enter aquatic environments and pose a risk to aquatic organisms. However, the potential threat and toxicological mechanisms of metamifop in aquatic organisms are poorly understood. In this study, zebrafish embryos were used to investigate the potential developmental toxicity and mechanisms of metamifop. The results showed that metamifop exhibited high acute toxicity to zebrafish, with 96 h-LC50 values of 0.648 and 0.216 mg/L to embryos and larvae of 72 h post-hatching (hph), respectively. Decreased body lengths, heartbeat number, and hatching rates, and increased malformation rates of embryos were observed after 96 h of exposure to 0.38 mg/L or higher concentration of metamifop. Furthermore, oxidative stress was caused in embryos, with increased contents of reactive oxygen species (ROS) and malondialdehyde (MDA), and altered activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Metamifop exposure clearly triggered cell apoptosis in embryos, result in the increase of Caspase-3 and Caspase-9 activities and up-regulation of apoptosis-related genes (bax, p53, apaf1, caspase-3, and caspase-9). Additionally, the transcriptions of innate immune-related genes (il-8, il-1b, and ifn) were increased in the groups treated with 0.25 and 0.5 mg/L of metamifop. These results indicate that metamifop induced developmental toxicity in zebrafish, and the potential toxicological mechanisms were related to oxidative stress, cell apoptosis, and the innate immune responses in embryos.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping