This study actually found out that you can experience a five-fold increase in your BPA levels, few hours after fiddling around with thermal paper. This is because the thermal paper on which the receipt is printed on contains alarmingly high levels of BPA as seen in this study. What’s even more troubling is the fact that in all of the studies I’ve seen, 95-99% of the test subjects had detectable levels of BPA in their system. E) This study saw that Bisphenol A inhibited the enzyme 5-alpha reductase, thus blocked dihydrotestosterone (DHT) production. D) This study found out that BPA causes sexual dysfunction in human males. Indeed, except for some factory workers with high occupational exposure, measured BPA levels in biological fluids are usually low and the hazards to fertility for the general population remain a matter for debate. An inhibitory effect on ΔΨm in human spermatozoa exposed to BPA has been also reported, even at very lower doses, in a subsequent study by Grami et al. (139). The disruption of CYP11A1 either involving the gene or protein expression decreases the conversion of cholesterol to pregnenolone in the mitochondria of LC. Furthermore, exposure to BPA at the same dose for 42 days also decreased the protein expression of CYP11A1 . Exposure to BPA at a dose of 200 mg/kg for 28 days reduced the gene expression of CYP11A1 in the testicular mitochondria of male Sprague-Dawley rats . The disturbance of the StAR mRNA expression may lead to the deterioration of testicular steroidogenesis due to the disturbance in cholesterol transportation and movement into the mitochondria in the LC. The gene and protein expression of StAR was decreased in adult male rats exposed to BPA for 28 days and 42 days, respectively, at a dose of 200 mg/kg by oral gavage 65,67. The disruption of BTB integrity may allow germ cells in the adluminal compartment to be exposed to toxicants, leading to the disturbance of spermatogenesis in the seminiferous tubules. The disturbances of these proteins lowered the integrity of BTB, which was proven by the reduction in cell viability and androgen receptor (AR) after 6 h of BPA exposure . A study carried out by Li et al. found a disturbance in the BTB of male Wistar rats, which was proven by the reduction of occludin and nectin-3 when exposed to BPA in a dose-dependent manner. BPA and its analogues were reported to disturb spermatogenesis by diminishing the BTB integrity, changing testicular histopathology, and causing sperm defects 52,64,65,66,67,68,69,70,75,76,77,80,81. However, the testosterone hormone helps release the mature spermatozoa into the lumen of the seminiferous tubule, thus preventing spermatozoa from being engulfed by the SC . Moreover, testosterone also plays an essential role in preventing the elongated spermatid from being released earlier. The germ cells, such as spermatogonia, spermatocyte, and spermatid, undergo various stages of spermatogenesis to form sperm. These results suggest that exposure to BPA enhances the RCT process in testicular tissues by up-regulating Apoa1, which in turn inhibits testosterone synthesis and secretion. (A) Detection of mice (A) testicular and (B) serum testosterone levels after BPA treatment. These results indicate that BPA exposure significantly inhibits testosterone synthesis and secretion in mice. This study will provide a new perspective on the mechanism through which BPA inhibits testosterone synthesis in mice by focusing on lipid metabolism. According to EFSA (49), apart from oral exposure, the skin contact with thermal paper represents a major source of exposure to BPA. While the estimated inhalation exposure would be negligible when compared to dietary route (38, 39), with the exception of some factory workers with high occupational exposure (40, 41), transdermal absorption should deserve special attention. This finding seems to be at the variance with the assumption that BPA is rapidly eliminated after ingestion and that the digestive tract represents the main source of exposure. The diminished sperm count after BPA exposure was confirmed by several other studies in rodents 83,91,94,95,96,97,98,99 and humans 76,100. In mice, males exposed to BPA by oral ingestion presented reduced testes and seminal vesicles weight, with a consequent reduction in sperm count . Moreover, BPA indirectly suppresses the release of LH through aromatase upregulation in testis, blocking testosterone synthesis. LH acts on Leydig cells and FSH on Sertoli cells, stimulating the biosynthesis of testosterone and inhibin B, respectively. All these alterations result in impaired testosterone production, with consequent effects on spermatogenesis 78,79 (Figure 1). (A–C) Detection of relative expression levels of genes to Apoa1, Apoa2, and Apoc3 in testicular tissues relative to the levels of the housekeeping gene Gapdh. Effect of BPA exposure on lipid droplets, cholesterol, and HDL in mice testis. Before euthanasia, blood samples were drawn by extirpating the eyeballs and centrifuged for serum preparation at 2000 xg for 15 min to assess serum testosterone levels. Primary Sertoli cell cultures exposed to intermediate doses of BPA (10 and 50 μM) showed increased GSH content due to increased GSH synthesis and recycling enzyme expression without affecting cell viability . In addition, the increased testicular ROS production may result in mitochondria dysfunction in Sertoli cells, leading to apoptosis . Indeed, in vitro exposure of human spermatozoa to BPA resulted in mitochondrial dysfunction (decreased MMP and increased mitochondrial generation of O2−) with a consequent reduction in sperm motility and increased DNA oxidative damage . The correlation between BPA exposure and alterations of sperm DNA was also observed in humans by evaluating the sperm DNA damage in a cohort of 190 subfertile male patients .
