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Cytogenetic and developmental toxicity of bisphenol A and bisphenol S in Arbacia lixula sea urchins embryos
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Researchers tested bisphenol A and bisphenol S for embryotoxicity and cytogenetic toxicity in Arbacia lixula sea urchin embryos at concentrations from 0.1 to 100 µM, evaluating developmental malformations, mitotic activity, and chromosome aberrations. They found both compounds caused embryotoxic effects from 2.5 µM upward, but bisphenol A produced approximately five-fold higher malformation rates than bisphenol S and was the only compound to induce cytogenetic anomalies.
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 developmental and cytogenetic toxicity endpoints. Embryonic malformations and/or mortality were scored to determine embryotoxicity (72 h post-fertilization, p-f). Cytogenetic toxicity was measured as mitotic activity endpoints and chromosome aberrations score in embryos (6 h p-f). 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 µM to 100 µM (with a ~5-fold difference). BP-A, not BP-S exhibited cytogenetic anomalies 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.
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