Korean J Anat.  2008 Sep;41(3):205-211.

Cytoprotective Effects of Serum Hormone Deprivation against Glutamate Toxicity in HT22 Mouse Hippocampal Cells

Affiliations
  • 1Department of Anatomy and Neurobiology, Medical Research Center for Neural Dysfunction, Institute of Health and Science, Gyeongsang National University School of Medicine, Jinju 660-751, Korea. choiws@gnu.ac.kr

Abstract

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.

Keyword

Reactive oxygen species; Glutamate; Cytotoxicity; HT22 cells

MeSH Terms

Acetylcysteine
Animals
Brain
Cell Line
Glutamic Acid
Heme Oxygenase-1
Mice
Neurons
Reactive Oxygen Species
Starvation
Acetylcysteine
Glutamic Acid
Heme Oxygenase-1
Reactive Oxygen Species
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