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N ‐acetylcysteine increases apoptosis induced by H 2 O 2 and mo‐antiFas triggering in a 3DO hybridoma cell line
Author(s) -
Lepri Enrica,
Gambelunghe Cristiana,
Fioravanti Alessandra,
Pedini Mauro,
Micheletti Alessandra,
Rufini Stefano
Publication year - 2000
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/1099-0844(200009)18:3<201::aid-cbf873>3.0.co;2-a
Subject(s) - acetylcysteine , apoptosis , intracellular , glutathione , programmed cell death , cell culture , microbiology and biotechnology , chemistry , antioxidant , cell , biology , biochemistry , genetics , enzyme
N ‐Acetylcysteine (NAC) has been used as an antioxidant to prevent apoptosis triggered by different stimuli in different cell types. It is common opinion that cellular redox, which is largely determined by the ratio of oxidized and reduced glutathione (GSH), plays a significant role in the propensity of cells to undergo apoptosis. However, there are also contrasting opinions stating that intracellular GSH depletion or supplemented GSH alone are not sufficient to lead cells to apoptosis or conversely protect them. Unexpectedly, this study shows that NAC, even if it maintains the peculiar characteristics of an agent capable of reducing cell proliferation and increasing intracellular GSH content, increases apoptosis induced by H 2 O 2 treatment and mo‐antiFas triggering in a 3DO cell line. We found that 24 h of NAC pre‐treatment can shift cellular death from necrotic to apoptotic and determine an early expression of FasL in a 3DO cell line treated with H 2 O 2 . Copyright © 2000 John Wiley & Sons, Ltd.