Reactive oxygen species (ROS) are important signaling molecules or mediators in many cellular responses, including the oxidative-burst defense response. Certain hormones are neuroprotective because they are modulators of neuronal activity or ROS scavengers. We have examined the effect of a hormone-free condition on ROS levels following glutamate-induced excitotoxicity in the mouse hippocampal HT22 cell line. We show that hormone starvation slightly elevates ROS and that continuous low concentrations of ROS induce expression of antioxidant enzymes, such as heme oxygenase-1 (HO-1). In addition, N-acetyl-L-cysteine (NAC) restores the expression of ERK1/2 protein in hormone-starved HT22 cells. These findings suggest that whereas high-dose ROS are cytotoxic and lead to tissue damage in the brain low-dose ROS may act in neuroprotective signaling.
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