| Butyl benzyl phthalate suppresses the ATP-induced cell proliferation in human osteosarcoma HOS cells. | |
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MedLine Citation:
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PMID: 20114058 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Butyl benzyl phthalate (BBP), an endocrine disruptor present in the environment, exerts its genomic effects via intracellular steroid receptors and elicits non-genomic effects by interfering with membrane ion-channel receptors. We previously found that BBP blocks the calcium signaling coupled with P2X receptors in PC12 cells (Liu & Chen, 2006). Osteoblast P2X receptors were recently reported to play a role in cell proliferation and bone remodeling. In this present study, the effects of BBP on ATP-induced responses were investigated in human osteosarcoma HOS cells. These receptors mRNA had been detected, named P2X4, P2X7, P2Y2, P2Y4, P2Y5, P2Y9, and P2Y11, in human osteosarcoma HOS cells by RT-PCR. The enhancement of cell proliferation and the decrease of cytoviability had both been shown to be coupled to stimulation via different concentrations of ATP. BBP suppressed the ATP-induced calcium influx (mainly coupled with P2X) and cell proliferation but not the ATP-induced intracellular calcium release (mainly coupled with P2Y) and cytotoxicity in human osteosarcoma HOS cells. Suramin, a common P2 receptor's antagonist, blocked the ATP-induced calcium signaling, cell proliferation, and cytotoxicity. We suggest that P2X is mainly responsible for cell proliferation, and P2Y might be partially responsible for the observed cytotoxicity. BBP suppressed the calcium signaling coupled with P2X, suppressing cell proliferation. Since the importance of P2X receptors during bone metastasis has recently become apparent, the possible toxic risk of environmental BBP during bone remodeling is a public problem of concern. |
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Authors:
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Pei-Shan Liu; Chih-Ying Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-01-28 |
Journal Detail:
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Title: Toxicology and applied pharmacology Volume: 244 ISSN: 1096-0333 ISO Abbreviation: Toxicol. Appl. Pharmacol. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-05 Completed Date: 2010-04-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0416575 Medline TA: Toxicol Appl Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 308-14 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Microbiology, Soochow University, Shihlin, Taipei, Taiwan, ROC. pslediting@mail.scu.edu.tw |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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antagonists & inhibitors* Bone Neoplasms Calcium Signaling / drug effects Cell Line, Tumor Cell Proliferation / drug effects* Endocrine Disruptors / toxicity* Growth Inhibitors / toxicity* Humans Osteoblasts / cytology, drug effects*, metabolism Osteosarcoma Phthalic Acids / toxicity* RNA, Messenger / metabolism Receptors, Purinergic P2 / drug effects, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Endocrine Disruptors; 0/Growth Inhibitors; 0/Phthalic Acids; 0/RNA, Messenger; 0/Receptors, Purinergic P2; 0/purinergic P2X receptor; 56-65-5/Adenosine Triphosphate; 85-68-7/butylbenzyl phthalate |
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