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α‐tocopherol protects PC12 cells From hyperoxia‐induced apoptosis
Author(s) -
Takahashi Hideo,
Kosaka Naoko,
Nakagawa Shigeki
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980415)52:2<184::aid-jnr6>3.0.co;2-6
Subject(s) - hyperoxia , apoptosis , dna fragmentation , programmed cell death , tocopherol , fragmentation (computing) , microbiology and biotechnology , vitamin e , lactate dehydrogenase , cell culture , biology , chemistry , antioxidant , oxygen , biochemistry , genetics , enzyme , ecology , organic chemistry
Abstract A rat clonal pheochromocytoma cell line (PC12) was cultured under normoxic (21% O 2 ) and hyperoxic (50% O 2 ) conditions. PC12 cells underwent apoptotic cell death when they were cultured in charcoal‐stripped medium in a high‐oxygen atmosphere. Vitamin E homologs, α‐tocopherol (αT), β‐tocopherol (βT), γ‐tocopherol (γT), and δ‐tocopherol (δT), were added to the culture medium to study their biological activities. αT was more effective than γT and δT in preventing hyperoxia‐induced cell death. Addition of exogenous αT to charcoal‐treated medium prevented lactate dehydrogenase (LDH) leakage from PC12 cells and also inhibited the apoptosis, which was accompanied by DNA fragmentation. Additional αT was rapidly concentrated in PC12 cells, suggesting that it exerts antioxidant effects. Our data show that PC12 cell death under high‐oxygen conditions is due to apoptosis and that, among the vitamin E homologs, αT most effectively prevents hyperoxic apoptosis. J. Neurosci. Res. 52:184–191, 1998. © 1998 Wiley‐Liss, Inc.