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  • 1
    Digitale Medien
    Digitale Medien
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 72 (1999), S. 0 
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Effects of estrogen hormones on lipid peroxidation (LPO)were examined in rat brain homogenates (RBHs), hippocampal HT 22 cells, ratprimary 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 andHT 22 homogenates. Incubation of living rat primary neocortical cultures withiron resulted in an EC50 of 0.5 mM, whereas culturehomogenates showed an EC50 of 1.2 mM. Estrogen hormonesreduced LPO in all systems: In RBHs, estrone inhibited iron-induced LPO to74.1 ± 5.8% of control levels (17β-estradiol: 71.3 ± 0.1%)at a concentration of 10 μM. In hippocampal HT 22 cellhomogenates, levels of LPO were reduced to 74.8 ± 5.5% by estrone andto 47.8 ± 6.2% by 17β-estradiol. In living neocortical cultures,17β-estradiol decreased iron-induced LPO to 79.2 ± 4.8% andincreased the survival of cultured neuronal cells. Of the other steroidcompounds tested (corticosterone, progesterone, testosterone), onlyprogesterone decreased LPO in HT 22 cell homogenates. In HBHs, LPO wasdose-dependently increased by iron concentrations from 2.7 to 6.0 mM.Incubation with estrogens resulted in a dose-dependent inhibition of LPO to53.89 ± 8.6% with 10 μM 17β-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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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