Chronic cerebral hypoperfusion induces striatal alterations due to the transient increase of NO production and the depression of glutathione content.
We examined the effects of chronic cerebral hypoperfusion on the endogenous oxidative stress-related indices, nitrite and nitrate (NOx) concentration, glutathione (GSH) content, superoxide dismutase and catalase activities, and thiobarbituric acid-reactive substances level in the rat striatum, to clarify the participation of oxidative stress in the chronic cerebral hypoperfusion-induced alterations. Our present results indicate that chronic cerebral hypoperfusion produces oxidative stress and disturbs intracellular redox regulation in two distinct phases: at 1 day, "acute" and at 6 weeks, "chronic" alterations after the operation. Therefore, striatal neural cell damage may be mainly attributed to the transient increase of NOx production at 1 day after, and the delayed reduction of muscarinic acetylcholine receptor binding in the striatum may be mostly attributed to the continuous depression of GSH content from the 1st to the 6th postoperative week. In particular, the continuous GSH depression may be considered to accompany the pathophysiology of chronic cerebral hypoperfusion.
Tanaka
Ken-Ichi
K
Department of Brain Science, Okayama University Graduate School of Medicine and Dentistry, Japan. kntanaka@cc.okayama-u.ac.jp
Wada-Tanaka
Naoko
N
Miyazaki
Ikuko
I
Nomura
Masahiko
M
Ogawa
Norio
N
D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism*; D007700:Kinetics; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D010477:Perfusion; D051381:Rats
D009566:Nitrates; D009573:Nitrites; D009569:Nitric Oxide; D005978:Glutathione