Hyperoxidized peroxiredoxins and glyceraldehyde-3-phosphate dehydrogenase immunoreactivity and protein levels are changed in the gerbil hippocampal CA1 region after transient forebrain ischemia.
Oxidative stress is a major pathogenic event occurring in several brain disorders and is a major cause of brain damage due to ischemia/reperfusion. Thiol proteins are easily oxidized in cells exposed to reactive oxygen species (ROS). In the present study, we investigated transient ischemia-induced chronological changes in hyperoxidized peroxiredoxins (Prx-SO3) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH-SO3) immunoreactivity and protein levels in the gerbil hippocampus induced by 5 min of transient forebrain ischemia. Weak Prx-SO3 immunoreactivity is detected in the hippocampal CA1 region of the sham-operated group. Prx-SO3 immunoreactivity was significantly increased 12 h and 1 day after ischemia/reperfusion, and the immunoreactivity was decreased to the level of the sham-operated group 2 days after ischemia/reperfusion. Prx-SO3 immunoreactivity in the 4 days post-ischemia group was increased again, and the immunoreactivity was expressed in glial components for 5 days after ischemia/reperfusion. GAPDH-SO3 immunoreactivity was highest in the CA1 region 1 day after ischemia/reperfusion, the immunoreactivity was decreased 2 days after ischemia/reperfusion. Four days after ischemia/reperfusion, GAPDH-SO3 immunoreactivity increased again, and the immunoreactivity began to be expressed in glial components from 5 days after ischemia/reperfusion. Prx-SO3 and GAPDH-SO3 protein levels in the ischemic CA1 region were also very high 12 h and 1 day after ischemia/reperfusion and returned to the level of the sham-operated group 3 days after ischemia/reperfusion. Their protein levels were increased again 5 days after ischemia/reperfusion. In conclusion, Prx-SO3 and GAPDH-SO3 immunoreactivity and protein levels in the gerbil hippocampal CA1 region are significantly increased 12 h-24 h after ischemia/reperfusion and their immunoreactivity begins to be expressed in glial components from 4 or 5 days after ischemia/reperfusion.
Hwang
In Koo
IK
Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chuncheon 200-702, South Korea.
Yoo
Ki-Yeon
KY
Kim
Dae Won
DW
Choi
Jung Hoon
JH
Lee
In Se
IS
Won
Moo Ho
MH
D000818:Animals; D016923:Cell Death; D005849:Gerbillinae; D024601:Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+) / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000502:physiology; D010544:Peroxidases / Q000494:pharmacology*; D054464:Peroxiredoxins; D016548:Prosencephalon / Q000098:blood supply
D010544:Peroxidases; D054464:Peroxiredoxins; D024601:Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+)