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Gen Comp Endocrinol
2004 Sep 15;1383:228-36. doi: 10.1016/j.ygcen.2004.06.011.
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Effects of 17beta-estradiol, nonylphenol, and bisphenol-A on developing Xenopus laevis embryos.
Sone K
,
Hinago M
,
Kitayama A
,
Morokuma J
,
Ueno N
,
Watanabe H
,
Iguchi T
.
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Many chemicals released into the environment have the capacity to disrupt the normal development of aquatic animals. We investigated the influence of nonylphenol (NP), bisphenol-A (BPA), and 17beta-estradiol (E2) on developing Xenopus laevis embryos, as a model animal in the aquatic environment. Embryos were exposed to eight different concentrations of NP, BPA or E2 between 3 and 96 h post-fertilization (p.f.). Short body length, microcephaly, flexure, edema, and abnormal gut coiling were induced by 20 microM NP, BPA or 10 microM E2 by 96 h p.f. To clarify sensitive stages to these compounds, embryos were exposed to chemicals for 45 or 48 h starting at different developmental stages and experiments were terminated 96 h p.f. BPA and NP induced abnormalities in developing X. laevis, though the sensitive stages of embryos to these chemicals are different, BPA affecting earlier stages and NP affecting at later stages. To analyze the functional mechanisms of BPA and NP in induction of morphological changes, we adapted a DNA array technology and identified 6 X. laevis genes, XIRG, alpha skeletal tropomyosin, cyclin G1, HGF, troponin C2, and ribosomal protein L9. These findings may provide important clues to elucidate common mechanisms underlying teratogenic effects of these chemicals.
Fig. 1. Effects of nonylphenol (NP), bisphenol-A (BPA), and 17bestradiol
(E2) on developing X. laevis embryos. Percentages of
malformed (dark gray bars) and dead (light gray bars) tadpoles after
93h exposure to a series of concentrations of NP, BPA or E2.
Percentages of normally developed tadpoles are shown as black bars.
DMC and control indicate tadpoles were cultured in 0.1· Steinbergs
solution and medium with solvent only, respectively (final concentration
of ethanol was less than 0.1%).
Fig. 2. Malformed tadpoles induced by 93h exposure of 20lM NP (B, F, and J), 20lM BPA (C, G, and K), 20lM E2 (D, H, and L), and normal
tadpoles (A, E, and I) at stage 44. Malformed tadpoles show microcephaly, short body length, flexure abnormal gut coiling, and edema. Cross-section
of head (M, N, O, and P) and abdomen (Q, R, S, and T) of NP (N and R), BPA (O and S), E2 (P and T) exposed and normal tadpoles (M and Q).
CNS, central nervous system; no, notochord; ms, muscle.
Fig. 3. Effects of NP (20lM), BPA (20lM) or E2 (20lM) on body
length of tadpoles exposed 45 or 48h. Chemical exposure was started at
different developmental stage and body length were measured at 96h
p.f. Data were represented as percentages of body length of controls.
Means ± SEM (n = 3). *P < 0.05 vs. Control, **P < 0.01 vs. Control.
Significance was determined by ANOVA followed by Fishers PLSD
test.
Fig. 4. Induction of microcephaly by NP (20lM), BPA (20lM) or E2
(20lM). Chemicals were exposed for 45 or 48h from different
developmental stages. *P < 0.05 vs. Control, **P < 0.01 vs. Control.
Fig. 5. Induction of flexure by NP (20lM), BPA (20lM) or E2
(20lM). Chemicals were exposed for 45 or 48h from different
developmental stages. *P < 0.05 vs. DMC, **P < 0.01 vs. DMC.
Fig. 6. Induction of edema by NP (20lM), BPA (20lM) or E2
(20lM). Chemicals were exposed for 45 or 48h from different
developmental stages. *P < 0.05 vs. DMC, **P < 0.01 vs. DMC.
Fig. 7. Induction of abnormal gut coiling by NP (20lM), BPA
(20lM) or E2 (20lM). Chemicals were exposed for 45 or 48h from
different developmental stages. *P < 0.05 vs. DMC, **P < 0.01 vs.
DMC.
