Abstract：
:Arsenic is a well-known environmental toxicant but the mechanism by which it causes cytotoxicity is poorly understood. Arsenite induces apoptosis in glutathione (GSH)-deficient GCS-2 cells by causing cell cycle dysfunction and down-regulating critical signaling pathways. This study was designed to examine the effect of arsenite on redox-sensitive phosphatidylinositol 3-kinase (PI3K)/Akt, a signaling pathway involved in cell survival and growth, and transcription factor, activating protein-1 (AP-1). Arsenite significantly diminished Akt and c-Fos levels and caused accelerated degradation of these proteins by ubiquitnation. Arsenite also induced cell cycle arrest and apoptosis. The cell cycle arrest involved the down-regulation of cyclin A2, cyclin D1, cyclin E, cyclin dependent kinases (CDK) 2, CDK4, and CDK6. Apoptosis involved down-regulation of anti-apoptotic proteins Bcl-2, Bcl-xL, survivin, and inhibitor of apoptosis protein (IAP) and up-regulation of pro-apoptotic protein Bax. Taken together, our results suggest that a possible mechanism of arsenite-induced toxicity under low/no GSH conditions, is to negatively regulate GCS-2 cell proliferation by attenuating Akt and AP-1 by ubiquitination and causing cell cycle dysfunction and apoptosis.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Habib GMdoi
10.1002/jcb.22548subject
Has Abstractpub_date
2010-05-15 00:00:00pages
363-71issue
2eissn
0730-2312issn
1097-4644journal_volume
110pub_type
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