Oxidative stress has been involved in various neurological disorders and, i
n the central nervous system, astrocytes represent the cell type that contr
ibutes to neuroprotection via glutathione (GSH) metabolism, GSH-metabolizin
g enzymes like gamma-glutamyltransferase (GGT), and apoE secretion. In this
study, using IL-1 beta, a proinflammatory and prooxidant cytokine that is
increased in numerous pathological situations, cells of astrocytoma cell li
ne U373-MG were exposed to an oxidative stress, leading to c-Jun and c-Fos
activation. IL-1 beta decreased both GGT activity and intracellular GSH con
tent and increased apoE secretion, initiating astroglial response to injury
. We observed that antioxidants inhibit IL-1 beta effects on c-Jun and c-Fo
s proteins, GGT activity and the GSH pool but not on apoE secretion. Our re
sults allow us to conclude that neurological disorders associated with an I
L-1 beta-induced oxidative stress could be, at least experimentally, revers
ible in the presence of one antioxidant, N-acetylcysteine.