XB-ART-56076Data Brief August 1, 2019; 25 104091.
Data demonstrating distinct embryonic developmental defects induced by bisphenol a alternatives.
Embryos of Xenopus laevis (African clawed frog) were exposed to the widespread environmental plasticizers bisphenol AF (BPAF; 0.003-3 μM), bisphenol A (BPA; 1-50 μM), or 17β-estradiol (E2; 10 μM) from just after fertilization through 96 hours of development. The potencies and cellular and morphological effects were compared across chemical treatments and controls. The embryos were staged, counted and imaged, and time-lapse movies collected, on an inverted stereomicroscope and camera. The data show there were both shared and unique effects of BPAF, BPA, and E2, on early cleavage divisions and development of the spinal cord, head, and gut, with BPAF having the greatest potency and toxicity (1000 times more potent than BPA). Specifically, cleavage divisions, within 1-6 hours of exposure had severe irregularities including asymmetrical division, slowed mitosis and cytokinesis, cellular dissociation, and fewer numbers of cells per embryo. By 48 hours of exposure the embryos had curved body axis defects, neural tube defects including curved, incomplete, or two neural tubes, ventral and gut blisters, and overall extreme abnormalities. By 96 hours of exposure estradiol caused tail flexures/bent spines, severe pigmentation reduction, long loosely coiled gut, and a ventral blister in 100% of embryos. BPA caused truncated body axis defects, tail flexures, and head and eye malformations in over 60% of embryos. BPAF, at the lowest doses tested, caused craniofacial defects, shorter tails, ventral blisters, edema and peritoneal effusion in over 75% of the surviving embryos. For a complete description, interpretation of the data and a discussion refer to the article in press Arancio et al., 2018.
PubMed ID: 31249853
PMC ID: PMC6586600
Article link: Data Brief
GO keywords: neural tube development
Article Images: [+] show captions
|Fig. 1. Early cleavage division defects caused by BPA and BPAF. Control embryos (left column), compared to embryos exposed to BPA (50 μM; middle column) or BPAF (3 μM; right column) at 1, 2 and 6 hours of exposure. Irregular, asymmetrical mitotic division, slowed cytokinesis, and cellular dissociation were observed in the majority of BPA- and BPAF-treated embryos (arrows).|
|Fig. 2. Early embryological defects caused by E2, BPA, and BPAF. A) Control tailbud stage embryos at 48 hours of development compared to tadpoles exposed to 10 μM estradiol (B), BPA at 1 (C), 10 (D), and 25 μM (E), and BPAF at 0.03 μM (F), showing curved body axis defects, neural tube defects including two neural tubes, gut blisters, and overall extreme abnormalities (arrows; scale bar = 1 mm).|
|Fig. 3. Late embryological defects caused by E2, BPA, and BPAF. A) Control tadpole at 96 hours of development compared to tadpoles exposed to 10 μM estradiol (B), BPA at 10 (C) and 25 μM (D, E), and BPAF at 0.03 μM (F). E2 caused tail flexures, severe pigmentation reduction, long loosely coiled gut, and a ventral blister in 100% of embryos (arrows). BPA caused truncated body axis and body axis defects, bent tails, and head and eye defects (C–E, arrows). BPAF caused shorter tails, craniofacial defects, ventral blisters, edema and peritoneal effusion in over 90% of surviving embryos (F, arrows).|
Arancio, Bisphenol A, Bisphenol AF, di-n-butyl phthalate, and 17β-estradiol have shared and unique dose-dependent effects on early embryo cleavage divisions and development in Xenopus laevis. 2019, Pubmed, Xenbase