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 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.
Desjardins
G C
GC
Department of Anatomy, McGill University, Montreal, Quebec.
Beaudet
A
A
Schipper
H M
HM
Brawer
J R
JR
D000818:Animals; D004958:Estradiol / Q000009:adverse effects* / Q000494:pharmacology; D005260:Female; D007031:Hypothalamus / Q000737:chemistry* / Q000187:drug effects / Q000473:pathology; D007150:Immunohistochemistry; D009474:Neurons / Q000737:chemistry* / Q000187:drug effects* / Q000473:pathology; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000494:pharmacology*; D001615:beta-Endorphin / Q000032:analysis*
D014810:Vitamin E; D004958:Estradiol; D001615:beta-Endorphin