PUBLICATION
Methylmercury Induced Neurotoxicity and the Influence of Selenium in the Brains of Adult Zebrafish (Danio rerio)
- Authors
- Rasinger, J.D., Lundebye, A.K., Penglase, S.J., Ellingsen, S., Amlund, H.
- ID
- ZDB-PUB-170330-1
- Date
- 2017
- Source
- International Journal of Molecular Sciences 18(4): (Journal)
- Registered Authors
- Ellingsen, Ståle
- Keywords
- contaminant, dietary, exposure, interaction, mechanisms, mercury, methylmercury, nutrient, proteomics, selenium
- MeSH Terms
-
- Animals
- Brain/drug effects*
- Brain/metabolism
- Gap Junctions/metabolism
- Methylmercury Compounds/pharmacokinetics
- Methylmercury Compounds/toxicity*
- Mitochondria/drug effects
- Mitochondria/metabolism
- Oxidative Phosphorylation
- Reactive Oxygen Species/metabolism
- Selenomethionine/pharmacokinetics
- Selenomethionine/pharmacology*
- TOR Serine-Threonine Kinases/metabolism
- Water Pollutants/pharmacokinetics
- Water Pollutants/toxicity*
- Zebrafish
- PubMed
- 28353644 Full text @ Int. J. Mol. Sci.
Citation
Rasinger, J.D., Lundebye, A.K., Penglase, S.J., Ellingsen, S., Amlund, H. (2017) Methylmercury Induced Neurotoxicity and the Influence of Selenium in the Brains of Adult Zebrafish (Danio rerio). International Journal of Molecular Sciences. 18(4).
Abstract
The neurotoxicity of methylmercury (MeHg) is well characterised, and the ameliorating effects of selenium have been described. However, little is known about the molecular mechanisms behind this contaminant-nutrient interaction. We investigated the influence of selenium (as selenomethionine, SeMet) and MeHg on mercury accumulation and protein expression in the brain of adult zebrafish (Danio rerio). Fish were fed diets containing elevated levels of MeHg and/or SeMet in a 2 × 2 full factorial design for eight weeks. Mercury concentrations were highest in the brain tissue of MeHg-exposed fish compared to the controls, whereas lower levels of mercury were found in the brain of zebrafish fed both MeHg and SeMet compared with the fish fed MeHg alone. The expression levels of proteins associated with gap junction signalling, oxidative phosphorylation, and mitochondrial dysfunction were significantly (p < 0.05) altered in the brain of zebrafish after exposure to MeHg and SeMet alone or in combination. Analysis of upstream regulators indicated that these changes were linked to the mammalian target of rapamycin (mTOR) pathways, which were activated by MeHg and inhibited by SeMet, possibly through a reactive oxygen species mediated differential activation of RICTOR, the rapamycin-insensitive binding partner of mTOR.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping