title: Estrogen hormones reduce lipid peroxidation in cells and tissues of the central nervous system.
abstract: Effects of estrogen hormones on lipid peroxidation (LPO) were examined in rat brain homogenates (RBHs), hippocampal HT 22 cells, rat primary neocortical cultures, and human brain homogenates (HBHs). Dose-response curves indicated half-maximal effective concentrations (EC50) of 5.5 and 5.6 mM for iron-induced LPO in RBHs and HT 22 homogenates. Incubation of living rat primary neocortical cultures with iron resulted in an EC50 of 0.5 mM, whereas culture homogenates showed an EC50 of 1.2 mM. Estrogen hormones reduced LPO in all systems: In RBHs, estrone inhibited iron-induced LPO to 74.1 +/- 5.8% of control levels (17beta-estradiol: 71.3 +/- 0.1%) at a concentration of 10 microM. In hippocampal HT 22 cell homogenates, levels of LPO were reduced to 74.8 +/- 5.5% by estrone and to 47.8 +/- 6.2% by 17beta-estradiol. In living neocortical cultures, 17beta-estradiol decreased iron-induced LPO to 79.2 +/- 4.8% and increased the survival of cultured neuronal cells. Of the other steroid compounds tested (corticosterone, progesterone, testosterone), only progesterone decreased LPO in HT 22 cell homogenates. In HBHs, LPO was dose-dependently increased by iron concentrations from 2.7 to 6.0 mM. Incubation with estrogens resulted in a dose-dependent inhibition of LPO to 53.8 +/- 8.6% with 10 microM 17beta-estradiol, whereas estrone failed to affect iron-induced LPO to a significant extent. Nonestrogenic steroids, including hydrocortisol, did not show significant effects on LPO in HBHs.
authors.affiliation: Department of Psychiatry and Psychotherapy, Philipps University of Marburg, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Vedder
authors.forename: N
authors.initials: N
authors.lastname: Anthes
authors.forename: G
authors.initials: G
authors.lastname: Stumm
authors.forename: C
authors.initials: C
authors.lastname: Würz
authors.forename: C
authors.initials: C
authors.lastname: Behl
authors.forename: J C
authors.initials: JC
authors.lastname: Krieg
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002712:Chlorides; D003345:Corticosterone / Q000494:pharmacology*; D004958:Estradiol / Q000494:pharmacology*; D005290:Ferric Compounds / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D019579:Neocortex / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013739:Testosterone / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D002712:Chlorides; D005290:Ferric Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D008315:Malondialdehyde; C024555:ferric chloride; D003345:Corticosterone