Antral follicles are major producers of estrogen in the ovary and are also responsive to gonadotropin stimulation. These follicles will begin to die without proper hormonal stimuli. Specifically, follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol are major survival factors for antral follicles. Thus, it is possible that antral follicles may undergo an increased rate of atresia due to an alteration in hormones or because fewer antral follicles are available for estrogen production, which might in turn lead to altered levels of gonadotropins.
The purpose of this study was twofold, first to examine whether MXC-induced atresia occurred through alterations in Bcl-2 or Bax, and second, to examine the effect of MXC on selected hormone and/or receptor levels. Specifically, this work tested the hypothesis that Bcl-2 expression is downregulated and/or Bax expression is upregulated by MXC, and further that an increase in Bcl-2 protein expression would protect against MXC-induced atresia, and the elimination of Bax expression would protect against MXC-induced atresia. In addition, this work tested the hypothesis that MXC increased atresia by altering levels of estradiol, FSH, or LH, hormones vital to antral follicle survival or that MXC affects the levels of estrogen receptors and/or FSH receptors because the levels of these receptors are also important for follicular survival.