Files in this item



application/pdfMAHALINGAM-THESIS-2016.pdf (750kB)
(no description provided)PDF


Title:Equol inhibits growth, induces atresia, and inhibits steroidogenesis of mouse antral follicles
Author(s):Mahalingam, Sharada
Advisor(s):Flaws, Jodi
Department / Program:Comparative Biosciences
Discipline:VMS - Comparative Biosciences
Degree Granting Institution:University of Illinois at Urbana-Champaign
antral follicle
Abstract:Equol is a non-steroidal estrogen metabolite produced by microbial conversion of daidzein, a major isoflavone phytoestrogen in soybean, in the gut of some humans and many animal species. Previous studies indicate that isoflavones and their metabolites can affect endogenous estradiol production, action, and metabolism via several mechanisms, which could in turn influence ovarian follicle growth. However, no studies have examined the direct effects of equol on intact antral follicles, which are responsible for sex steroid synthesis and further development into ovulatory follicles. The present study tested the hypothesis that equol inhibits antral follicle growth, increases follicle atresia, and inhibits steroidogenesis in the adult mouse ovary. Ovarian antral follicles from adult CD-1 mice were cultured with vehicle control or equol (600 nM, 6 µM, 36 µM, 100 µM) for 48 and 96 h. Follicle diameters were measured every 24 h to monitor follicle growth, and at 48 and 96 h, follicles were subjected to gene expression analysis and media were subjected to measurement of hormone levels. Follicles were also subjected to western blot analysis of certain steroidogenic enzymes, as well as histological evaluation of atresia following 96 h of culture. Equol (100 µM) inhibited follicle growth and induced follicle atresia. Further, equol decreased the levels of estradiol, testosterone, androstenedione, and progesterone, and decreased mRNA levels of cholesterol side-chain cleavage, steroid 17-α-hydroxalase, and aromatase compared to control. Collectively, these data suggest that equol alters antral follicle function by inhibiting growth, increasing atresia, and inhibiting steroidogenesis.
Issue Date:2016-04-11
Rights Information:Copyright 2016 Sharada Mahalingam
Date Available in IDEALS:2016-07-07
Date Deposited:2016-05

This item appears in the following Collection(s)

Item Statistics