Studies have also suggested that BPA interferes with germ cell nest breakdown in animal models. In neonatally exposed lambs, low-dose BPA was reported to increase the incidence of multioocyte follicles ( Rivera et al. 2011 ). Similarly, in gestationally exposed macaques, dietary low-dose BPA exposure increased the number of oocytes present in secondary and antral follicles at birth, and continuous BPA exposure (measured < 1 ng/mL in maternal serum) increased the incidence of unenclosed oocytes ( Hunt et al. 2012 ). Further, in gestationally exposed CD-1 mice, low-dose BPA increased the number of unenclosed oocytes, whereas it decreased the number of primordial follicles in a dose-dependent manner ( Zhang HQ et al. 2012 ). In another study, Veiga-Lopez et al. (2013) reported that prenatal BPA exposure altered the fetal ovarian steroidogenic gene and microRNA expression that mediate gonadal differentiation and folliculogenesis in sheep. Collectively, these studies provide strong evidence that gestational BPA exposure—across multiple exposure routes, doses, and species—impairs proper germ cell nest breakdown, leading to the formation of multioocyte follicles. The presence of multioocyte follicles is of concern because they are considered a pathologic condition that may lead to ovulatory problems ( Iguchi et al. 1990 ).
The StAR protein was first identified, characterized and named by Dr. Douglas Stocco at Texas Tech University Health Sciences Center in 1994.  The role of this protein in lipoid CAH was confirmed the following year in collaboration with Dr. Walter Miller at the University of California, San Francisco .  All of this work follows the initial observations of the appearance of this protein and its phosphorylated form coincident with factors that caused steroid production by Dr. Nanette Orme-Johnson while at Tufts University .