Japanese medaka (Oryzias latipes) exposed via maternal transfer to the brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO), experience decreased fecundity and impaired oocyte maturation.

Endocrine disruption Fecundity Maternal transfer Oocyte maturation Oogenesis

Journal

Aquatic toxicology (Amsterdam, Netherlands)
ISSN: 1879-1514
Titre abrégé: Aquat Toxicol
Pays: Netherlands
ID NLM: 8500246

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 29 08 2023
revised: 20 10 2023
accepted: 08 11 2023
pubmed: 20 11 2023
medline: 20 11 2023
entrez: 19 11 2023
Statut: ppublish

Résumé

Early life-stage exposure of fishes to endocrine disrupting chemicals can induce reproductive impairment at sexual maturity. Previously, we demonstrated decreased fecundity of Japanese medaka (Oryzias latipes) exposed via maternal transfer to the novel brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO). However, that study failed to identify the causative mechanism. In other studies we have shown that decreased fecundity of adult fish exposed to dietary TBCO is likely due to impaired oocyte maturation. The goal of the present study was to determine if impaired oocyte maturation is responsible for decreased fecundity of Japanese medaka exposed as embryos to TBCO, via maternal transfer. Sexually mature fish (F0) were fed either a control diet or a low (74.7 μg/g) or high (663 μg/g) diet containing TBCO for 21 days. Eggs (F1) were collected during the final week of exposure and reared to sexual maturity at which point fecundity was assessed using a 21-day reproduction assay. Upon termination of the assay, an ex vivo oocyte maturation assay was used to determine whether maturation inducing hormone (MIH) stimulated oocyte maturation was impaired. Additionally, concentrations of 17β -estradiol (E2) in blood plasma and expression of genes involved in vitellogenesis and oocyte maturation were quantified. The F1 generation females reared from the low or high F0 treatments experienced a 26.0 % and 56.8 % decrease in cumulative fecundity, respectively. Ex vivo MIH stimulated oocyte maturation from the low and high TBCO treatments were decreased by 23.4 % and 20.0 % respectively. There was no significant effect on concentrations of E2. Transcript abundance of vtgI was significantly decreased in a concentration dependent manner. Transcript abundance of mPRα, pgrmc1, pgrmc2, and igf3 were decreased but effects were not statistically significant. Overall, results suggest that impaired oocyte maturation causes decreased fecundity of Japanese medaka exposed to maternally deposited TBCO.

Identifiants

pubmed: 37980850
pii: S0166-445X(23)00363-6
doi: 10.1016/j.aquatox.2023.106761
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106761

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Chloe Devoy (C)

Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta T1K 3M4, Canada.

Yamin Raza (Y)

Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta T1K 3M4, Canada.

Paul D Jones (PD)

School of Environment and Sustainability, and The Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5C9, Canada.

Jon A Doering (JA)

Department of Environmental Sciences, Louisiana State University, Baton Rouge, LA 70803, United States.

Steve Wiseman (S)

Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta T1K 3M4, Canada. Electronic address: steve.wiseman@uleth.ca.

Classifications MeSH