ArticleEcotoxicology (London, England)2022
Cytogenetic and developmental toxicity of bisphenol A and bisphenol S in Arbacia lixula sea urchin embryos.
Article in Ecotoxicology (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Pregnancy and lactation exposure to bisphenol S induces ferroptosis via disrupted hepatic lipid metabolism in offspring mice.Frontiers in toxicology · 2026Article
- Developmental bisphenol S toxicity in two freshwater animal models.Environmental toxicology and pharmacology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol S (BP-S) is one of the most important substitutes of bisphenol A (BP-A), and its environmental occurrence is predicted to intensify in the future. Both BP-A and BP-S were tested for adverse effects on early life stages of Arbacia lixula sea urchins at 0.1 up to 100 µM test concentrations, by evaluating cytogenetic and developmental toxicity endpoints. Embryonic malformations and/or mortality were scored to determine embryotoxicity (72 h post-fertilization). It has been reported in academic dataset that bisphenols concentration reached μg/L in aquatic environment of heavily polluted areas. We have chosen concentrations ranging from 0.1-100 μM in order to highlight, in particular, BP-S effects. Attention should be paid to this range of concentrations in the context of the evaluation of the toxicity and the ecological risk of BP-S as emerging pollutant. Cytogenetic toxicity was measured, using mitotic activity and chromosome aberrations score in embryos (6 h post-fertilization). Both BP-A and BP-S exposures induced embryotoxic effects from 2.5 to 100 µM test concentrations as compared to controls. Malformed embryo percentages following BP-A exposure were significantly higher than in BP-S-exposed embryos from 0.25 to 100 µM (with a ~5-fold difference). BP-A, not BP-S exhibited cytogenetic toxicity at 25 and 100 µM. Our results indicate an embryotoxic potential of bisphenols during critical periods of development with a potent rank order to BP-A vs. BP-S. Thus, we show that BP-A alternative induce similar toxic effects to BP-A with lower severity.
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Registered trials
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 Socratic graph.