Fetal-Perinatal Exposure to Bisphenol-A Affects Quality of Spermatozoa in Adulthood Mouse

Abstract

Bisphenol-A (BPA) is considered an endocrine disruptor with estrogenic activity. It is described as an environment-polluting industrial chemical whose adverse effects on the male reproductive system depend on the period of exposure (i.e., fetal, prepubertal, or adult life). We exposed male mice to BPA during the fetal-perinatal period (from 10 days post coitum to 31 days post partum) and investigated the impact of this early-life exposure on gamete health in adulthood animals at 78 days of age. Both in control and BPA-exposed mice, viability and motility of spermatozoa, as well as sperm motility acquisition and chromatin condensation of spermatozoa, have been evaluated. Results reveal harmful effect of BPA on viability and motility of sperm cells as well as on chromatin condensation status during epididymal maturation of spermatozoa. In particular, BPA exposure interferes with biochemical mechanism useful to stabilize sperm chromatin condensation, as it interferes with oxidation of thiol groups associated to chromatin.

Temporal Trend of Conventional Sperm Parameters in a Sicilian Population in the Decade 2011–2020

“…Particularly, endocrine disruptors, heavy metals, chemicals, and lifestyle factors can impact testicular development and function starting from a prenatal age. As an example, fetal exposure to bisphenol-A, a chemical with estrogenic activity, disrupted spermatogenesis damaging viability, motility, and sperm chromatin condensation of adult mice [ 36 ]. The negative impact of this chemical on human fertility has been already ascertained [ 37 ], as well as that of phthalates [ 38 ].…”

Characterization of Estrogenic Activity and Site-Specific Accumulation of Bisphenol-A in Epididymal Fat Pad: Interfering Effects on the Endocannabinoid System and Temporal Progression of Germ Cells

“…Tissues collected from adult male mice early exposed to BPA, during foetal/perinatal period, were previously used for studies on biology of food intake and epididymal sperm maturation [ 17 , 36 , 42 ], here used to verify our hypothesis.…”

“…Consequently, exposure to BPA has been linked to developmental, systemic, reproductive, neurological and immune disorders in both humans and animals [ 23 , 24 ]. Impairment of spermatogenesis and functional sperm parameters, including germ cell proliferation [ 25 ], steroidogenesis [ 26 , 27 , 28 , 29 , 30 , 31 , 32 ], blood-testicular barrier (BTB) junctions [ 33 , 34 ], acrosome and spermatid differentiation [ 35 ], as well as mitochondrial function, chromatin condensation and integrity, number, motility and vitality of spermatozoa (SPZs) [ 21 , 36 , 37 , 38 ] are among the main interfering effects of BPA, documented so far in several animal models, including mice and rats, exposed pre/post-birth to low/high doses of BPA [ 26 ].…”

“…Consistently, we have recently reported that early exposure to BPA doses below the not observed-adverse effect levels (NOEL) value during the foetal/perinatal period, induces anorexigenic phenotype in prepubertal males with effects in adulthood on body weight and pEWAT adiposity [ 42 ]. Interestingly, these animals also showed sustained sperm death in caput epididymis, with no effects in cauda [ 36 ]. The molecular characterization of the anorexigenic phenotype in exposed animals revealed that BPA exerted agonistic estrogenic effects and counteracted the endogenous orexigenic activity of the ECS by interfering with the hypothalamic expression of ECS components [ 42 ].…”

“…Here, using tissues collected from the same batch of animals early exposed to BPA described above [ 17 , 36 ], we have characterized the estrogenic activity of BPA and verified the effects on testicular expression of ECS as a potential cause of impairment of spermatogenesis and sperm death in epididymal caput .…”