Journal
TOXICOLOGY LETTERS
Volume 206, Issue 3, Pages 300-305Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2011.08.011
Keywords
Bisphenol A; Derivatives; Hyperactivity; Endocrine disruptors
Categories
Funding
- NIES [12510]
- Grants-in-Aid for Scientific Research [21200025] Funding Source: KAKEN
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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 mu g 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. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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