Evidence map›Paper›PMID 33450672›Full record

ArticleAquatic toxicology (Amsterdam, Netherlands)2021

Assessing effects of aromatase inhibition on fishes with group-synchronous oocyte development using western mosquitofish (Gambusia affinis) as a model.

Jon A Doering, Daniel L Villeneuve, Charlene B Tilton, Ashley R Kittelson, Brett R Blackwell, Michael D Kahl, Kathleen M Jensen, Shane T Poole, Jenna E Cavallin, Alexander R Cole and 3 more

Open access · greenAbstract read
In one paragraph

Article in Aquatic toxicology (Amsterdam, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Frontiers in microbiology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Jon A DoeringNational Research Council, 6201 Congdon Boulevard, Duluth, MN, 55804, United States. Electronic address: jad929@mail.usask.ca.
Daniel L VilleneuveGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Charlene B TiltonOak Ridge Institute of Science Education, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Ashley R KittelsonOak Ridge Institute of Science Education, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Brett R BlackwellGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Michael D KahlGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Kathleen M JensenGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Shane T PooleGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Jenna E CavallinGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Alexander R ColeOak Ridge Institute of Science Education, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Kendra N DeanOak Ridge Institute of Science Education, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Carlie A LaLoneGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Gerald T AnkleyGreat Lakes Toxicology and Ecology Division, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, MN, 55804, United States.
Environmental Protection Agency · USNational Academies of Sciences, Engineering, and Medicine · US

Funding

Intramural EPA EPA999999
6 · The paper itself

Abstract

Exposure to certain anthropogenic chemicals can inhibit the activity to cytochrome P450 aromatase (CYP19) in fishes leading to decreased plasma 17β-estradiol (E2), plasma vitellogenin (VTG), and egg production. Reproductive dysfunction resulting from exposure to aromatase inhibitors has been extensively investigated in several laboratory model species of fish. These model species have ovaries that undergo asynchronous oocyte development, but many fishes have ovaries with group-synchronous oocyte development. Fishes with group-synchronous oocyte development have dynamic reproductive cycles which typically occur annually and are often triggered by complex environmental cues. This has resulted in a lack of test data and uncertainty regarding sensitivities to and adverse effects of aromatase inhibition. The present study used the western mosquitofish (Gambusia affinis) as a laboratory model to investigate adverse effects of chemical aromatase inhibition on group-synchronous oocyte development. Adult female western mosquitofish were exposed to either 0, 2, or 30 μg/L of the model nonsteroidal aromatase inhibiting chemical, fadrozole, for a complete reproductive cycle. Fish were sampled at four time-points representing pre-vitellogenic resting, early vitellogenesis, late vitellogenesis/early ovarian recrudescence, and late ovarian recrudescence. Temporal changes in numerous reproductive parameters were measured, including gonadosomatic index (GSI), plasma sex steroids, and expression of selected genes in the brain, liver, and gonad that are important for reproduction. In contrast to fish from the control treatment, fish exposed to 2 and 30 μg/L of fadrozole had persistent elevated expression of cyp19 in the ovary, depressed expression of vtg in the liver, and a low GSI. These responses suggest that completion of a group-synchronous reproductive cycle was unsuccessful during the assay in fish from either fadrozole treatment. These adverse effects data show that exposure to aromatase inhibitors has the potential to cause reproductive dysfunction in a wide range of fishes with both asynchronous and group-synchronous reproductive strategies.

Indexed as

Adverse outcome pathwayEndocrine disruptionFadrozoleSpecies extrapolation

Identifiers

PMID33450672
PMCPMC8255332
OpenAlexW3119917632

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.