ESTROGEN-DEPENDENT MODULATION OF RAT-BRAIN ASCORBATE LEVELS AND ISCHEMIA-INDUCED ASCORBATE LOSS

Citation
J. Kumekick et Me. Rice, ESTROGEN-DEPENDENT MODULATION OF RAT-BRAIN ASCORBATE LEVELS AND ISCHEMIA-INDUCED ASCORBATE LOSS, Brain research, 803(1-2), 1998, pp. 105-113
Citations number
55
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
803
Issue
1-2
Year of publication
1998
Pages
105 - 113
Database
ISI
SICI code
0006-8993(1998)803:1-2<105:EMORAL>2.0.ZU;2-J
Abstract
Brain ascorbate levels in young adult female rat are lower than those in males. Loss of ascorbate during ischemia is also less in females, s uggesting lower oxidative stress. After ovariectomy, however, ischemia -induced loss equals that in males. In the present study, we determine d ascorbate levels in maturing male and female rat brain to establish when the gender difference in content arises. We further investigated whether 17 beta-estradiol and/or progesterone treatment modulate level s and ischemia-induced loss in ovariectomized females and compared the se data with those from normal females in proestrus and estrus. Gender differences in brain ascorbate content were absent before: puberty an d persisted only in cortex in aging rats. Chronic estradiol treatment, whether alone or in combination with progesterone, prevented an ovari ectomy-induced ascorbate increase in hippocampus and caused levels in cortex and cerebellum to fall below those of randomly sampled normal f emales. These same low levels were found during proestrus and estrus. Estradiol replacement after ovariectomy prevented enhanced ischemia-in duced ascorbate loss in hippocampus, but not in cortex or cerebellum. Ischemia-induced losses in proestrus and estrus were similar to those in normal controls. Progesterone had little effect in any region. Thes e data indicate that ascorbate content and redox balance in female bra in are influenced postpubertally by estrogens in a region-selective ma nner. (C) 1998 Published by Elsevier Science B.V. All rights reserved.