PUBLICATION
In vitro and in vivo studies of oxidative stress responses against acrylamide toxicity in zebrafish
- Authors
- Komoike, Y., Matsuoka, M.
- ID
- ZDB-PUB-181127-13
- Date
- 2018
- Source
- Journal of hazardous materials 365: 430-439 (Journal)
- Registered Authors
- Keywords
- Acrylamide, Intracellular stress response signaling pathway, Oxidative stress, PCR array analysis, Zebrafish
- MeSH Terms
-
- Acrylamide/toxicity*
- Animals
- Cell Death/drug effects
- Cell Line
- In Vitro Techniques
- Oxidative Stress/drug effects*
- Oxidative Stress/genetics
- Reactive Oxygen Species/metabolism*
- Zebrafish
- PubMed
- 30453236 Full text @ J. Hazard. Mater.
Citation
Komoike, Y., Matsuoka, M. (2018) In vitro and in vivo studies of oxidative stress responses against acrylamide toxicity in zebrafish. Journal of hazardous materials. 365:430-439.
Abstract
Acrylamide (AA) is widely used in soil stabilization, water treatment, and industrial products and found in certain foods; however, its toxicity is an expanding global concern. Thus, to reveal the mechanisms involved in the development of, or protection from AA-induced toxicity has important significance. For this purpose, here we explored the intracellular stress response signaling pathways activated by AA exposure in zebrafish model. BRF41 cells derived from zebrafish were exposed to AA, and changes in the expression levels of 31 genes, including endoplasmic reticulum stress response-, oxidative stress response-, osmotic stress response-, and DNA damage and repair-related genes, were analyzed by PCR array. 12 genes upregulated in AA-exposed BRF41 cells were analyzed in zebrafish larvae by quantitative real time PCR, and the expression of all tested oxidative stress response-related genes was upregulated. Spatial expression patterns of these genes were visualized and found that their expression was upregulated and ectopically induced. In addition, AA-induced toxicity in BRF41 cells and the expression of glutathione S-transferase pi 1 (gstp1) in zebrafish larvae were reduced by N-acetylcysteine. Furthermore, inhibition of Gst activity enhanced AA toxicity. From these results, we concluded that the elicited oxidative stress response critically contributes to the protection from AA-induced toxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping