Journal
NEUROSCIENCE LETTERS
Volume 353, Issue 2, Pages 99-102Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/j.neulet.2003.09.031
Keywords
bisphenol A; nonylphenol; programmed cell death; caspase-3
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We examined whether bisphenol A (BPA) and 4-nonylphenol (NP) influenced staurosporine-induced neuronal cell death in primary cultured rat hippocampal and cortical neurons. In hippocampal neurons, 17beta-estradiol (E-2) (1 nM and 10 muM) and BPA (10 muM) significantly inhibited the staurosporine-induced release of lactate dehydrogenase (LDH). In cortical neurons, BPA significantly inhibited the LDH release, while E-2 did not. In hippocampal neurons, E-2 and BPA significantly inhibited the staurosporine-induced increase in caspase-3 activity. In cortical neurons, BPA and NP significantly inhibited the increase in caspase-3 activity, while E-2 did not. Furthermore, low-dose BPA (10 nM) also significantly inhibited the increase in caspase-3 activity in both hippocampal and cortical neurons. BPA and NP might impede normal brain development by inhibiting even desirable neuronal cell death, interfering with caspase-3 activation. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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