In vivo assay of the ethanol-induced embryonic hair cell loss and the protective role of the retinoic and folic acid in zebrafish larvae (Danio rerio).
Animals
Animals, Genetically Modified
Dose-Response Relationship, Drug
Embryo, Nonmammalian
/ drug effects
Ethanol
/ toxicity
Female
Folic Acid
/ administration & dosage
Hair Cells, Auditory
/ drug effects
Pregnancy
Prenatal Exposure Delayed Effects
/ chemically induced
Tretinoin
/ administration & dosage
Zebrafish
Ethanol
Folic acid
Hair cell
Retinoic acid
Toxicity
Journal
Alcohol (Fayetteville, N.Y.)
ISSN: 1873-6823
Titre abrégé: Alcohol
Pays: United States
ID NLM: 8502311
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
04
11
2017
revised:
15
06
2018
accepted:
19
07
2018
pubmed:
15
1
2019
medline:
27
3
2020
entrez:
15
1
2019
Statut:
ppublish
Résumé
In reference to the auditory manifestation of fetal alcohol syndrome, previous work has preferentially focused on the deviant neural development of the auditory system. Changes in the sensory hair cell, the ultimate sensory organ, were not well understood. In this study, we carried out an in vivo assessment of the embryonic hair cell changes on the lateral line of zebrafish upon exposure to various ethanol concentrations (0.25%, 0.5%, 0.75%, and 1.0%). A significant decrease in the hair cell count was confirmed as the ethanol concentration increased. Long-term observation (up to 240 hours post-fertilization [hpf]) suggested an irreversible hair cell loss with little chance of a simple delayed development. For an underlying biological process, a significant increase of hair cell apoptosis and a significant decrease of cytoplasmic mitochondria were confirmed as the ethanol concentration increased. Co-treatment with retinoic (0.1 nM) or folic (0.1 mM) acid with the same concentrations of ethanol resulted in significant increases in the remaining hair cells, compared to the ethanol-only treatment group, for every ethanol concentration. The retinoic acid provided more effective protection over folic acid, resulting in no significant changes in hair cell counts for every ethanol concentration (except 1.0%), compared with that of the negative control (without chemical treatment). Hair cell counts in every ethanol concentration were significantly lower than those in negative controls without chemical treatment after folic acid co-treatment. In conclusion, gestational ethanol exposure causes developmental sensory hair cell loss. Potential underlying mechanisms include retinoic or folic acid deficiency, and mitochondrial damage with subsequent hair cell apoptosis. Hair cell loss could possibly be prevented by administering either retinoic or folic acid, with retinoic acid supplementation as the preferred treatment.
Identifiants
pubmed: 30640074
pii: S0741-8329(17)30943-6
doi: 10.1016/j.alcohol.2018.07.008
pii:
doi:
Substances chimiques
Ethanol
3K9958V90M
Tretinoin
5688UTC01R
Folic Acid
935E97BOY8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
113-121Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.