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NAD+ induces C6 glioma cell death by generating oxidative stress and increasing intracellular calcium concentrations
Author(s) -
Zhao Cuiping,
Chen Heyu,
Xia Weiliang,
Li Shengtian,
Ying Weihai
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb470
Subject(s) - nad+ kinase , oxidative stress , programmed cell death , calcium in biology , intracellular , calcium , bapta , glioma , trolox , chemistry , microbiology and biotechnology , biology , apoptosis , biochemistry , cancer research , enzyme , organic chemistry , antioxidant capacity
NAD+ plays important roles in various biological processes. We have found that while it is highly protective against oxidative stress‐induced death of primary neuronal cultures and astrocyte cultures, NAD+ can induce glioma and neuroblastoma cell death. In this study we investigated the mechanisms underlying the effects of NAD+ on C6 glioma cells. We found that two antioxidants, Trolox and N‐acetyl cysteine, can markedly decreased the NAD+‐induced glioma cell death, suggesting that oxidative stress mediates the effects of NAD+ on the cell death. Our study has also shown that BAPTA‐AM, a calcium chelator, also largely prevented NAD+‐induced decreases in the cell survival, suggesting a critical role of elevated intracellular calcium concentrations in the cell death. Collectively, our study has provided novel evidence that NAD+ treatment can induce oxidative stress and impaired calcium homeostasis in such tumor cell types as C6 glioma cells, which leads to decreased survival of the tumor cells. (Supported by a Key Basic Research Grant from Shanghai Educational Committee (to WY) and by a Pujiang Scholar Award (to WY)).