TY - JOUR
T1 - Acute restraint stress induces rapid changes in central redox status and protective antioxidant genes in rats
AU - Spiers, Jereme G.
AU - Chen, Hsiao Jou Cortina
AU - Cuffe, James S.M.
AU - Sernia, Conrad
AU - Lavidis, Nickolas A.
N1 - Publisher Copyright:
© 2016.
PY - 2016/5/1
Y1 - 2016/5/1
N2 - The stress-induced imbalance in reduction/oxidation (redox) state has been proposed to play a major role in the etiology of neurological disorders. However, the relationship between psychological stress, central redox state, and potential protective mechanisms within specific neural regions has not been well characterized. In this study, we have used an acute psychological stress to demonstrate the dynamic changes that occur in the redox system of hippocampal and striatal tissue. Outbred male Wistar rats were subject to 0 (control), 60, 120, or 240 min of acute restraint stress and the hippocampus and striatum were cryodissected for redox assays and relative gene expression. Restraint stress significantly elevated oxidative status and lipid peroxidation, while decreasing glutathione ratios overall indicative of oxidative stress in both neural regions. These biochemical changes were prevented by prior administration of the glucocorticoid receptor antagonist, RU-486. The hippocampus also demonstrated increased glutathione peroxidase 1 and 4 antioxidant expression which was not observed in the striatum, while both regions displayed robust upregulation of the antioxidant, metallothionein 1a. This was observed with concurrent upregulation of 11β-hydroxysteroid dehydrogenase 1, a local reactivator of corticosterone, in addition to decreased expression of the cytosolic regulatory subunit of superoxide-producing enzyme, NADPH-oxidase. Together, this study demonstrates distinctive regional redox profiles following acute stress exposure, in addition to identifying differential capabilities in managing oxidative challenges via altered antioxidant gene expression in the hippocampus and striatum.
AB - The stress-induced imbalance in reduction/oxidation (redox) state has been proposed to play a major role in the etiology of neurological disorders. However, the relationship between psychological stress, central redox state, and potential protective mechanisms within specific neural regions has not been well characterized. In this study, we have used an acute psychological stress to demonstrate the dynamic changes that occur in the redox system of hippocampal and striatal tissue. Outbred male Wistar rats were subject to 0 (control), 60, 120, or 240 min of acute restraint stress and the hippocampus and striatum were cryodissected for redox assays and relative gene expression. Restraint stress significantly elevated oxidative status and lipid peroxidation, while decreasing glutathione ratios overall indicative of oxidative stress in both neural regions. These biochemical changes were prevented by prior administration of the glucocorticoid receptor antagonist, RU-486. The hippocampus also demonstrated increased glutathione peroxidase 1 and 4 antioxidant expression which was not observed in the striatum, while both regions displayed robust upregulation of the antioxidant, metallothionein 1a. This was observed with concurrent upregulation of 11β-hydroxysteroid dehydrogenase 1, a local reactivator of corticosterone, in addition to decreased expression of the cytosolic regulatory subunit of superoxide-producing enzyme, NADPH-oxidase. Together, this study demonstrates distinctive regional redox profiles following acute stress exposure, in addition to identifying differential capabilities in managing oxidative challenges via altered antioxidant gene expression in the hippocampus and striatum.
KW - Acute stress
KW - Glucocorticoid receptor
KW - Glutathione peroxidase
KW - Oxidative stress
KW - RU-486
KW - Redox status
UR - http://www.scopus.com/inward/record.url?scp=84962508618&partnerID=8YFLogxK
U2 - 10.1016/j.psyneuen.2016.02.005
DO - 10.1016/j.psyneuen.2016.02.005
M3 - Article
SN - 0306-4530
VL - 67
SP - 104
EP - 112
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
ER -