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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-kappaB.
J Neurosci Res. 2008 Oct; 86(13):2932-42.JN

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 microM. 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)-kappaB. Pretreatment with specific inhibitors for calcium, ROS, ERK, and JNK decreased BPA-induced cell death; however, inhibitor for NF-kappaB 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-kappaB cascade was activated for survival signaling after BPA treatment.

Authors+Show Affiliations

CMRI, Department of Pharmacology, School of Medicine, Kyungpook National University, Joong-gu, Daegu, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18521933

Citation

Lee, Soyoung, et al. "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-kappaB." Journal of Neuroscience Research, vol. 86, no. 13, 2008, pp. 2932-42.
Lee S, Suk K, Kim IK, et al. 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-kappaB. J Neurosci Res. 2008;86(13):2932-42.
Lee, S., Suk, K., Kim, I. K., Jang, I. S., Park, J. W., Johnson, V. J., Kwon, T. K., Choi, B. J., & Kim, S. H. (2008). 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-kappaB. Journal of Neuroscience Research, 86(13), 2932-42. https://doi.org/10.1002/jnr.21739
Lee S, et al. 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-kappaB. J Neurosci Res. 2008;86(13):2932-42. PubMed PMID: 18521933.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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-kappaB. AU - Lee,Soyoung, AU - Suk,Kyoungho, AU - Kim,In Kyeom, AU - Jang,Il-Sung, AU - Park,Jin-Woo, AU - Johnson,Victor J, AU - Kwon,Taeg Kyu, AU - Choi,Byung-Ju, AU - Kim,Sang-Hyun, PY - 2008/6/4/pubmed PY - 2008/12/31/medline PY - 2008/6/4/entrez SP - 2932 EP - 42 JF - Journal of neuroscience research JO - J Neurosci Res VL - 86 IS - 13 N2 - 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 microM. 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)-kappaB. Pretreatment with specific inhibitors for calcium, ROS, ERK, and JNK decreased BPA-induced cell death; however, inhibitor for NF-kappaB 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-kappaB cascade was activated for survival signaling after BPA treatment. SN - 1097-4547 UR - https://www.unboundmedicine.com/medline/citation/18521933/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_kappaB_ L2 - https://doi.org/10.1002/jnr.21739 DB - PRIME DP - Unbound Medicine ER -