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Title: Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH-SY5Y cell
Authors: Piyajit Watcharasit
Sumitra Suntararuks
Daranee Visitnonthachai
Apinya Thiantanawat
Jutamaad Satayavivad
Chulabhorn Research Institute
Chulabhorn Graduate Institute
Mahidol University
Keywords: Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Oct-2010
Citation: Journal of Applied Toxicology. Vol.30, No.7 (2010), 649-655
Abstract: Acrylonitrile (ACN) is a chemical that is widely used in the production of plastics, acrylic fibers, synthetic rubbers and resins. It has been reported that ACN can cause oxidative stress, a condition which is well recognized as an apoptotic initiator; however, information regarding ACN-induced apoptosis is limited. This present study investigated whether ACN induces apoptosis in human neuroblastoma SH-SY5Y cells, and whether its apoptotic induction involves oxidative stress. The results showed that ACN caused activation of caspase-3, a key enzyme involved in apoptosis, in a dose- and time-dependent manner. Detection of sub-G1 apoptotic cell death and apoptotic nuclear condensation revealed that ACN caused an increase in the number of apoptotic cells indicating ACN induces apoptosis in SH-SY5Y cells. ACN dose- and time-dependently increased the level of proapoptotic protein, Bax. Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells. Moreover, induction of Bax by ACN was abolished by NAC. Taken together, the results indicate that ACN induces apoptosis in SH-SY5Y cells via a mechanism involving generation of oxidative stress-mediated Bax induction. Copyright © 2010 John Wiley & Sons, Ltd.
ISSN: 10991263
Appears in Collections:Scopus 2006-2010

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