Premium
Cellular glucose‐6‐phosphate dehydrogenase (G6PD) status modulates the effects of nitric oxide (NO) on human foreskin fibroblasts
Author(s) -
Cheng Mei-ling,
Ho Hung-yao,
Liang Chi-ming,
Chou Yi-hung,
Stern Arnold,
Lu Fung-jou,
Chiu Daniel Tsun-yee
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01687-2
Subject(s) - foreskin , nitric oxide , sodium nitroprusside , apoptosis , trolox , glucose 6 phosphate dehydrogenase , chemistry , microbiology and biotechnology , cell growth , stimulation , dehydrogenase , cell , biology , biochemistry , endocrinology , cell culture , oxidative stress , enzyme , genetics , antioxidant capacity
Glucose‐6‐phosphate dehydrogenase (G6PD) plays an important role in cellular redox homeostasis, which is crucial for cell survival. In the present study, we found that G6PD status determines the response of cells exposed to nitric oxide (NO) donor. Treatment with NO donor, sodium nitroprusside (SNP), caused apoptosis in G6PD‐deficient human foreskin fibroblasts (HFF1), whereas it was growth stimulatory in the normal counterpart (HFF3). Such effects were abolished by NO scavengers like hemoglobin. Ectopic expression of G6PD in HFF1 cells switched the cellular response to NO from apoptosis to growth stimulation. Experiments with 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one and 8‐bromo‐cGMP showed that the effects of NO on HFF1 and HFF3 cells were independent of cGMP signalling pathway. Intriguingly, trolox prevented the SNP‐induced apoptosis in HFF1 cells. These data demonstrate that G6PD plays a critical role in regulation of cell growth and survival.