Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Toxicol Lett. 2011 Oct 30;206(3):300-5. doi: 10.1016/j.toxlet.2011.08.011. Epub 2011 Aug 22.

Rat hyperactivity by bisphenol A, but not by its derivatives, 3-hydroxybisphenol A or bisphenol A 3,4-quinone.

Author information

  • 1Center for Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506, Japan. ishidou@nies.go.jp

Abstract

Detoxification in the central nervous system is largely unknown. The mechanism of neurotoxicity of bisphenol A, a toxic environmental chemical remains obscure. We examined the effects of bisphenol A, and its derivatives, 3-hydroxybisphenol A and bisphenol A 3,4-quinone on rat behavior as possible metabolites of bisphenol A. A single intracisternal administration of bisphenol A (20 μg equivalent to 87 nmol) into 5-day-old male Wistar rats caused significant hyperactivity at 4-5 weeks of age. It was about 1.3 fold more active in the nocturnal phase than control rats. However, neither 3-hydroxybisphenol A nor bisphenol A 3,4-quinone at the same amount (87 nmol) increased the spontaneous motor activity. Gas chromatographic-mass spectrometric (GC-MS) analyses of the treated brain revealed that 7% of the parent chemical resided in the brain at 8 weeks of age, but its derivatives were not found. This suggested a difference in metabolic turnover of these compounds or a difference in their stabilities. We conclude that bisphenol A per se caused hyperactivity in the rat, eliminating the possibility that possible metabolic forms of bisphenol A, 3-hydroxybisphenol A and bisphenol A 3,4-quinone have the ability to elicit rat hyperactivity, probably because of longer-lasting residence of the parent compound in the brain.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

PMID:
21884766
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk