Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity

Estradiol valerate (EV) treatment has been shown to result in the destruction of 60% of beta-endorphin neurons in the hypothalamic arcuate nucleus. Evidence suggests that the mechanism of EV-induced neurotoxicity involves the conversion of estradiol to catechol estrogen and subsequent oxidation to f...

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Bibliographic Details
Published inEndocrinology (Philadelphia) Vol. 131; no. 5; p. 2482
Main Authors Desjardins, G C, Beaudet, A, Schipper, H M, Brawer, J R
Format Journal Article
LanguageEnglish
Published United States 01.11.1992
Subjects
Animals
beta-Endorphin - analysis
Estradiol - adverse effects
Estradiol - pharmacology
Female
Hypothalamus - chemistry
Hypothalamus - drug effects
Hypothalamus - pathology
Immunohistochemistry
Neurons - chemistry
Neurons - drug effects
Neurons - pathology
Radioimmunoassay
Rats
Rats, Wistar
Vitamin E - pharmacology
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Summary:Estradiol valerate (EV) treatment has been shown to result in the destruction of 60% of beta-endorphin neurons in the hypothalamic arcuate nucleus. Evidence suggests that the mechanism of EV-induced neurotoxicity involves the conversion of estradiol to catechol estrogen and subsequent oxidation to free radicals in local peroxidase-positive astrocytes. In this study, we examined whether treatment with the antioxidant, vitamin E, protects beta-endorphin neurons from the neurotoxic action of estradiol. Our results demonstrate that chronic vitamin E treatment prevents the decrement in hypothalamic beta-endorphin concentrations resulting from arcuate beta-endorphin cell loss, suggesting that the latter is mediated by free radicals. Vitamin E treatment also prevented the onset of persistent vaginal cornification and polycystic ovarian condition which have been shown to result from the EV-induced hypothalamic pathology.
ISSN:0013-7227
DOI:10.1210/en.131.5.2482