PUBLICATION
Paraquat exposure induces behavioral deficits in larval zebrafish during the window of dopamine neurogenesis
- Authors
- Nellore, J., P, N.
- ID
- ZDB-PUB-171002-3
- Date
- 2015
- Source
- Toxicology reports 2: 950-956 (Journal)
- Registered Authors
- Keywords
- ADHD, attention deficient hyperactivity disorder, Cholinergic system, DTNB, 5 5′-dithiobis-(2- nitrobenzoic acid), EM, embryo medium, Early life, GSH, glutathione, LPO, lipid peroxidation, Motor defects, PD, Parkinson’s disease, PQ, paraquat, Paraquat, hpf, hours post fertilization, ppm, parts per million
- MeSH Terms
- none
- PubMed
- 28962434 Full text @ Toxicol Rep
Citation
Nellore, J., P, N. (2015) Paraquat exposure induces behavioral deficits in larval zebrafish during the window of dopamine neurogenesis. Toxicology reports. 2:950-956.
Abstract
Exposure to environmental risk factors such as herbicides in early life has been proposed to play important roles in the development of neurodegenerative disorders in adult life. To test this hypothesis, we used a zebrafish model to link the herbicide paraquat (PQ) to disease etiology. Strikingly, treatment of 18 hpf embryonic zebrafish with low-dose PQ treatment (0.04 ppm, lower than the accepted human daily exposure) resulted in 50% display of neurodegenerative phenotypes and motor deficits at various developmental stages (segmentation to larval stage). Wide arrays of biomarkers have been employed to delineate the toxic responses which include lipid peroxidation, glutathione (GSH) and apoptosis studies. A decrease in the GSH levels, increase in lipid peroxidation and apoptosis, respectively, were observed at various developmental stages. Unexpectedly, we show that the exposure to paraquat during the window of dopamine neurogenesis causes Parkinsonian like motor defects in later life by perturbing cholinergic system due to oxidative stress.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping