During stress exposure, the glucocorticoid-driven increase in cellular metabolism enhances reactive oxygen species formation from the inner mitochondrial electron transfer chain. This results in a tissue specific induction of oxidative stress that subsequently alters the overall redox status. In the brain, the hippocampus has demonstrated a particular susceptibility to stress-induced oxidative stress. However, the temporal relationship between an increase in glucocorticoids and redox changes in the hippocampus has not been defined. In this study, male Wistar rats were randomly divided into control, 60, 120, or 240 minute stress groups (n=9). Blood samples were collected at 0 (baseline) minutes, and immediately following the cessation of stress treatment. Whole blood samples were used for glucose determination while plasma was stored for later analysis of corticosterone, redox status, and lipid peroxidation. The hippocampus was cryo-dissected and stored at -80^oC prior to assays for oxidative status, the glutathione redox couple, lipid peroxidation, and relative gene expression of the antioxidant genes MT1A and GPx1. Baseline blood glucose significantly increased at 60 and 120 minutes, and fell below baseline by 240 minutes of stress. Plasma corticosterone concentrations also increased approximately 400% consistently, while redox status and lipid peroxidation continually increased over the duration of the experiment. Hippocampal oxidative status and lipid peroxidation initially increased at 60 minutes while the glutathione redox ratio was decreased, together indicating oxidative stress. However, following 120 and 240 minutes of stress recovery was evident. Relative gene expression of the antioxidant gene MT1A continually increased after 120 minutes while GPx1 was unaffected. It was concluded that acute restraint stress, through corticosterone, increases central and peripheral indicators of oxidative stress while concurrently increasing the central expression of specific protective antioxidant genes. Further studies of the functional significance of these specific gene products should elucidate their role in oxidative susceptibility during acute restraint stress.