Exposure to bisphenol A (BPA), even at environmentally low doses, disrupts the preovulatory luteinizing hormone (LH) surge and leads to abnormal estrous cycle and folliculogenesis, according to a study recently published in Endocrinology. This disruption is reversible following adult exposure, but it persists into adulthood after neonatal exposure.
Researchers led by David Lopez-Rodriguez, MSc, at the neuroendocrinology laboratory of AnneSimone Parent, MD, PhD, (GIGA-Neuroscience), the University of Liege, Belgium, point out that BPA is found in almost everything, even though it has been partially banned in some countries. Humans are exposed to BPA through food and drink, and several studies have implicated BPA in contaminating fetuses and neonates. “Sex steroids play a crucial role perinatally in ‘organizing’ the control of female reproduction,” the authors write. “For that reason, the adult female estrous cycle is altered following exogenous exposure to sex steroids during that vulnerable perinatal period. Therefore, the effects of early exposure to BPA on puberty and reproduction are a matter of concern.”
The researchers note that they have already shown that exposure to BPA can delay or advance vaginal opening, through a low or high dose, respectively. For this study, the authors write, they wanted to see whether neonatal exposure to a low dose of BPA could produce persistent disruption of folliculogenesis and estrous cycle that could be consistent with disturbed organization. “We also used the high BPA dose because opposing effects on GnRH secretion and pubertal timing were seen after using the low and the high doses of BPA neonatally,” they write. “Finally, the aim was to evaluate whether adult BPA exposure in similar conditions would produce persistent or transient effects on ovulation and folliculogenesis.”
The team injected one-day-old and 90-day-old rats with either corn oil or BPA (a high dose or a low dose) for 15 days. Neonatal exposure to both doses disrupted the estrous cycle and folliculogenesis, a disruption that persisted into adulthood. Both doses given to adults caused a reversible decrease in antral follicles and corpora lutea as well as a reversible disruption of the estrous cycle associated with a delay and a decrease in the amplitude of the LH surge was also observed, according to the authors. “Although the alterations of estrous cyclicity persist after neonatal exposure, they appear to be transient during adult exposure to BPA,” the authors write. “During 2 weeks of adult exposure to a very low or high dose of BPA, altered estrous cyclicity occurs together with disruption of the late stages of folliculogenesis (antral follicles and corpora lutea). Importantly, all of these effects appear to have disappeared 1 month after stopping the exposure to BPA.”
“In conclusion,” the authors write, “we show that both adult and neonatal exposure to a very low dose of BPA in the range of nanograms can result in alteration of estrous cyclicity and folliculogenesis.” They go on to write that their findings show that when further evaluating BPA’s effects on the female reproductive axis, very low doses should be used, while including the neonatal period and addressing neuroendocrine and ovarian endpoints.
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