PUBLICATION
Evaluation of okadaic acid toxicity in human retinal cells and zebrafish retinas
- Authors
- Tchivelekete, G.M., Almarhoun, M., Cao, Y., Zhou, X., Martin, P.E., Shu, X.
- ID
- ZDB-PUB-220517-25
- Date
- 2022
- Source
- Toxicology 473: 153209 (Journal)
- Registered Authors
- Keywords
- ARPE-19 cells, Inflammation, Neurotoxicity, Okadaic acid, Oxidative stress, Zebrafish embryos
- MeSH Terms
-
- Retina
- Oxidative Stress*
- Humans
- Inflammation
- Zebrafish*
- Okadaic Acid/toxicity
- Animals
- PubMed
- 35577138 Full text @ Toxicology
- CTD
- 35577138
Citation
Tchivelekete, G.M., Almarhoun, M., Cao, Y., Zhou, X., Martin, P.E., Shu, X. (2022) Evaluation of okadaic acid toxicity in human retinal cells and zebrafish retinas. Toxicology. 473:153209.
Abstract
Okadaic acid (OA, C₄₄H₆₈O₁₃) is a neurotoxin and phosphatase inhibitor produced by several dinoflagellate species. OA is widely known to accumulate in black sponges and is associated with seafood poisoning. Humans can be exposed to OA by consuming contaminated shellfish that have accumulated toxins during algal blooms. Evidence from in vitro and in vivo studies demonstrate that OA exposure causes neurotoxicity in addition to diarrheal syndrome. It is unclear whether exposure to OA affects retinal function, a part of the central nervous system. We evaluated the toxicity of OA in human retinal pigment epithelial cells (ARPE-19) and in zebrafish retinas. Cell-based assays determined that OA significantly decreased cell viability in a dose-dependent manner and increased oxidative stress, inflammation and cell death compared to the untreated control group. In the in vivo study, zebrafish embryos at 24hours post fertilization (hpf) were treated with/without OA for five days, endpoint measurements including mortality, malformations, delayed hatching, altered heartbeat and reduced movement were performed. OA exposure increased mortality, decreased hatching, heartbeat rate, and caused morphological abnormalities. OA exposure also markedly decreased the expression of antioxidant genes and a significantly increased inflammation as well as evoking a loss of photoreceptors in zebrafish embryos. The data suggest that consuming OA-contaminated seafood can induce retinal toxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping