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Acrylonitrile induced apoptosis via oxidative stress in neuroblastoma SH‐SY5Y cell
Author(s) -
Watcharasit Piyajit,
Suntararuks Sumitra,
Visitthachai Daranee,
Thiantanawat Apinya,
Satayavivad Jutamaad
Publication year - 2010
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1535
Subject(s) - apoptosis , oxidative stress , sh sy5y , chemistry , acrylonitrile , programmed cell death , caspase 3 , caspase , microbiology and biotechnology , cell culture , biology , biochemistry , neuroblastoma , polymer , organic chemistry , copolymer , genetics
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.