Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity

• Published in: Endocrinology (Philadelphia) Vol. 131; no. 5; p. 2482
• Main Authors: Desjardins, G C, Beaudet, A, Schipper, H M, Brawer, J R
• Format: Journal Article
• Language: English
• 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
• DOI: 10.1210/en.131.5.2482
• ISSN: 0013-7227

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.