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Signaling pathways of bisphenol A-induced apoptosis in hippocampal neuronal cells: role of calcium-induced reactive oxygen species, mitogen-activated protein kinases, and nuclear factor-kappa B.

Authors
Lee-S; Suk-K; Kim-IK; Jang-IS; Park-JW; Johnson-VJ; Kwon-TK; Choi-BJ; Kim-SH
Source
J Neurosci Res 2008 Oct; 86(13):2932-2942
NIOSHTIC No.
20034691
Abstract
In the present study, we investigated the neurotoxicity of bisphenol A [BPA; 2,2-bis-(4 hydroxyphenyl) propane] and the underlying mechanisms of action in mouse hippocampal HT-22 cells. BPA, known to be a xenoestrogen, is used in the production of water bottles, cans, and teeth suture materials. BPA-treated HT-22 cells showed lower cell viability than did controls at concentrations of BPA over 100 mu M. BPA induced apoptotic cell death as indicated by staining with Hoechst 33258, costaining with Annexin V/propidium iodide, and activation of caspase 3. BPA regulated the generation of reactive oxygen species (ROS) by increasing intracellular calcium. BPA activated phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), and nuclear translocation of nuclear factor (NF)-kappa B. Pretreatment with specific inhibitors for calcium, ROS, ERK, and JNK decreased BPA-induced cell death; however, inhibitor for NF-kappa B increased BPA-induced cell death. The results suggest that calcium, ROS, ERK, and JNK are involved in BPA-induced apoptotic cell death in HT-22 cells. In contrast, an NF-kappa B cascade was activated for survival signaling after BPA treatment.
Keywords
Animal-studies; Animals; Laboratory-animals; Hydroxyl-groups; Hydroxy-compounds; Laboratory-animals; Laboratory-testing; Cell-biology; Cellular-reactions; Cell-damage; Toxicology; Toxins; Neuropathology; Neurotoxic-effects; Neurotoxicology; Neurotoxins
Contact
Sang-Hyun Kim, Department of Pharmacology, Kyungpook National University Medical School, 101 Dong-In, Joong-gu, Daegu, 700-422, Republic of Korea
CODEN
JNREDK
CAS No.
80-05-7
Publication Date
20081001
Document Type
Journal Article
Email Address
shkim72@knu.ac.kr
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
13
ISSN
0360-4012
NIOSH Division
HELD
Source Name
Journal of Neuroscience Research
State
WV
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