Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis

Tomohiro Oka, Naoki Adati, Tadashi Shinkai, Keiko Sakuma, Tetsuji Nishimura, Kouichi Kurose

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Bisphenol A (BPA), known to be a xenoestrogen, is widely used in industry and dentistry. In the present study, we investigated the effects of BPA on the early development of Xenopus laevis embryos. Stage 6 embryos were exposed to 10-100μM BPA. Developmental abnormalities were observed when the embryos were exposed to at least 20μM BPA, with marked developmental abnormalities, such as crooked vertebrae and developmental defects of the head and abdomen, detected in all embryos up to stage 40. Interestingly, apoptosis occurred specifically in central nervous tissue cells of the brain and spinal cord, as assessed by histological analysis. BPA-induced malformations and apoptosis were not observed in embryos exposed to BPA after stage 10. When embryos were exposed to 10μM 17β-estradiol (E2), abnormalities were also observed until stage 40. However, the abnormalities induced by BPA and E2 were different and E2 exposure did not induce apoptosis in the central nervous system. Our results indicated that the developmental abnormalities and apoptosis induced by BPA exposure were not inhibited by the addition of E2. In conclusion, we demonstrated that BPA induced marked malformations and specific apoptosis of central nervous system cells during early development of X. laevis embryos, and that these BPA effects appeared to be due to non-estrogenic activities on developmental processes.

Original languageEnglish
Pages (from-to)877-882
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume312
Issue number4
DOIs
Publication statusPublished - 2003 Dec 26
Externally publishedYes

Fingerprint

Apoptosis
Neurology
bisphenol A
Dentistry
Estradiol
Brain
Tissue
Defects

Keywords

  • 17β-Estradiol
  • Amphibian
  • Apoptosis
  • Bisphenol A
  • Brain
  • Central nerve cell
  • Early development
  • Embryo
  • Endocrine disruptors
  • Estrogen receptor
  • Exposure test
  • Histological analysis
  • Malformation
  • TUNEL
  • Xenoestrogen
  • Xenopus laevis

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis. / Oka, Tomohiro; Adati, Naoki; Shinkai, Tadashi; Sakuma, Keiko; Nishimura, Tetsuji; Kurose, Kouichi.

In: Biochemical and Biophysical Research Communications, Vol. 312, No. 4, 26.12.2003, p. 877-882.

Research output: Contribution to journalArticle

Oka, Tomohiro ; Adati, Naoki ; Shinkai, Tadashi ; Sakuma, Keiko ; Nishimura, Tetsuji ; Kurose, Kouichi. / Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis. In: Biochemical and Biophysical Research Communications. 2003 ; Vol. 312, No. 4. pp. 877-882.
@article{d09b0d5c4a3c46ecbd67b717d43e51a4,
title = "Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis",
abstract = "Bisphenol A (BPA), known to be a xenoestrogen, is widely used in industry and dentistry. In the present study, we investigated the effects of BPA on the early development of Xenopus laevis embryos. Stage 6 embryos were exposed to 10-100μM BPA. Developmental abnormalities were observed when the embryos were exposed to at least 20μM BPA, with marked developmental abnormalities, such as crooked vertebrae and developmental defects of the head and abdomen, detected in all embryos up to stage 40. Interestingly, apoptosis occurred specifically in central nervous tissue cells of the brain and spinal cord, as assessed by histological analysis. BPA-induced malformations and apoptosis were not observed in embryos exposed to BPA after stage 10. When embryos were exposed to 10μM 17β-estradiol (E2), abnormalities were also observed until stage 40. However, the abnormalities induced by BPA and E2 were different and E2 exposure did not induce apoptosis in the central nervous system. Our results indicated that the developmental abnormalities and apoptosis induced by BPA exposure were not inhibited by the addition of E2. In conclusion, we demonstrated that BPA induced marked malformations and specific apoptosis of central nervous system cells during early development of X. laevis embryos, and that these BPA effects appeared to be due to non-estrogenic activities on developmental processes.",
keywords = "17β-Estradiol, Amphibian, Apoptosis, Bisphenol A, Brain, Central nerve cell, Early development, Embryo, Endocrine disruptors, Estrogen receptor, Exposure test, Histological analysis, Malformation, TUNEL, Xenoestrogen, Xenopus laevis",
author = "Tomohiro Oka and Naoki Adati and Tadashi Shinkai and Keiko Sakuma and Tetsuji Nishimura and Kouichi Kurose",
year = "2003",
month = "12",
day = "26",
doi = "10.1016/j.bbrc.2003.10.199",
language = "English",
volume = "312",
pages = "877--882",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "4",

}

TY - JOUR

T1 - Bisphenol A induces apoptosis in central neural cells during early development of Xenopus laevis

AU - Oka, Tomohiro

AU - Adati, Naoki

AU - Shinkai, Tadashi

AU - Sakuma, Keiko

AU - Nishimura, Tetsuji

AU - Kurose, Kouichi

PY - 2003/12/26

Y1 - 2003/12/26

N2 - Bisphenol A (BPA), known to be a xenoestrogen, is widely used in industry and dentistry. In the present study, we investigated the effects of BPA on the early development of Xenopus laevis embryos. Stage 6 embryos were exposed to 10-100μM BPA. Developmental abnormalities were observed when the embryos were exposed to at least 20μM BPA, with marked developmental abnormalities, such as crooked vertebrae and developmental defects of the head and abdomen, detected in all embryos up to stage 40. Interestingly, apoptosis occurred specifically in central nervous tissue cells of the brain and spinal cord, as assessed by histological analysis. BPA-induced malformations and apoptosis were not observed in embryos exposed to BPA after stage 10. When embryos were exposed to 10μM 17β-estradiol (E2), abnormalities were also observed until stage 40. However, the abnormalities induced by BPA and E2 were different and E2 exposure did not induce apoptosis in the central nervous system. Our results indicated that the developmental abnormalities and apoptosis induced by BPA exposure were not inhibited by the addition of E2. In conclusion, we demonstrated that BPA induced marked malformations and specific apoptosis of central nervous system cells during early development of X. laevis embryos, and that these BPA effects appeared to be due to non-estrogenic activities on developmental processes.

AB - Bisphenol A (BPA), known to be a xenoestrogen, is widely used in industry and dentistry. In the present study, we investigated the effects of BPA on the early development of Xenopus laevis embryos. Stage 6 embryos were exposed to 10-100μM BPA. Developmental abnormalities were observed when the embryos were exposed to at least 20μM BPA, with marked developmental abnormalities, such as crooked vertebrae and developmental defects of the head and abdomen, detected in all embryos up to stage 40. Interestingly, apoptosis occurred specifically in central nervous tissue cells of the brain and spinal cord, as assessed by histological analysis. BPA-induced malformations and apoptosis were not observed in embryos exposed to BPA after stage 10. When embryos were exposed to 10μM 17β-estradiol (E2), abnormalities were also observed until stage 40. However, the abnormalities induced by BPA and E2 were different and E2 exposure did not induce apoptosis in the central nervous system. Our results indicated that the developmental abnormalities and apoptosis induced by BPA exposure were not inhibited by the addition of E2. In conclusion, we demonstrated that BPA induced marked malformations and specific apoptosis of central nervous system cells during early development of X. laevis embryos, and that these BPA effects appeared to be due to non-estrogenic activities on developmental processes.

KW - 17β-Estradiol

KW - Amphibian

KW - Apoptosis

KW - Bisphenol A

KW - Brain

KW - Central nerve cell

KW - Early development

KW - Embryo

KW - Endocrine disruptors

KW - Estrogen receptor

KW - Exposure test

KW - Histological analysis

KW - Malformation

KW - TUNEL

KW - Xenoestrogen

KW - Xenopus laevis

UR - http://www.scopus.com/inward/record.url?scp=0344495435&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0344495435&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2003.10.199

DO - 10.1016/j.bbrc.2003.10.199

M3 - Article

VL - 312

SP - 877

EP - 882

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 4

ER -