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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Jan 28, 2014

Bisphenol A, or BPA is used in the linings of food and beverage cans. Researchers exposed
the developing testis in mice and saw that sperm in exposed animals did a poorer job of
meiosis, in which cells combine the genes of both parents. After exposure, sperm died.




BPA and estradiol affect sperm development

Washington State University researchers have found a direct link between the plastics component bisphenol A, or BPA, and disrupted sperm production. The chemical disrupts the delicate DNA interactions needed to create sperm which might explain declining sperm counts.

The work was published in the journal PLOS Genetics.

WSU geneticist and principle investigator Pat Hunt says she and her team may have unearthed the physiological mechanism that could account for decreased sperm counts seen in several human studies. It also bolsters the "estrogen hypothesis" that estrogen disruptors in the environment are at play.

"This provides some real insight into what exactly might be going on," Hunt says. "It's kind of bizarre because we got into it through a back door, not really starting out to look at that question."

In addition to seeing BPA effects, Hunt and her colleagues saw an even larger effect on sperm by estradiol, the birth control hormone that passes untreated through sewage plants.

Hunt has a long history of working with BPA, which is often found in plastic bottles, the linings of food and beverage cans, and thermal receipts. Much of her work has documented its effect on female reproduction, from mice to monkeys.

Declining sperm counts have been a subject of concern and conjecture since the early 1990s, when Danish researchers reported "a genuine decline in semen quality over the past 50 years," with possible implications for male fertility. Sperm count studies have often been criticized for being small, having biased populations or questionable statistical methods, but reproductive biologists continue to see data suggesting that endocrine disruptors like BPA, plastic-softening phthalates and estradiol are impairing reproduction. In a 2013 study cited by Hunt and her colleagues, French researchers looked at the partners of more than 26,000 infertile women and saw their semen concentration drop nearly 2 percent a year for 17 years.

In the WSU study, Hunt and her colleagues gave newborn male mice oral doses of BPA. They also exposed mice to the synthetic estrogen ethinyl estradiol. The researchers exposed the developing testis and saw that the sperm of exposed animals did a poorer job of meiosis, the process in which cells combine the genetic information of their parents. As a result, more sperm died.

"We have a window of just a few days and we permanently change the way that the testis makes sperm in the adult," says Hunt.

The study looked at three mice populations: one outbred like humans and two other, very common strains that are inbred. The researchers saw a "very strong effect" on outbred mice and one inbred strain, said Hunt, and no effect on the other inbred strain. Hunt said this would account for earlier researchers not seeing an effect on testes in earlier studies.

"This mouse model would suggest that here's actually a reason why these sperm counts would be falling," Hunt said. "We're actually doing something to this process that's going to cause the death of more cells as they're trying to make sperm. They're going to get culled out by this quality-control mechanism and the upshot of that will be that if you do enough of this, you'll drop sperm counts."

Hunt also worries that sperm counts will continue to go down with each exposed generation.

"We've seen effects over the course of several decades. What about several generations? Infertility is becoming more common. Are we creating the perfect storm?"

Bisphenol A (BPA) and other endocrine disrupting chemicals have been reported to induce negative effects on a wide range of physiological processes, including reproduction. In the female, BPA exposure increases meiotic errors, resulting in the production of chromosomally abnormal eggs. Although numerous studies have reported that estrogenic exposures negatively impact spermatogenesis, a direct link between exposures and meiotic errors in males has not been evaluated. To test the effect of estrogenic chemicals on meiotic chromosome dynamics, we exposed male mice to either BPA or to the strong synthetic estrogen, ethinyl estradiol during neonatal development when the first cells initiate meiosis. Although chromosome pairing and synapsis were unperturbed, exposed outbred CD-1 and inbred C3H/HeJ males had significantly reduced levels of crossovers, or meiotic recombination (as defined by the number of MLH1 foci in pachytene cells) by comparison with placebo. Unexpectedly, the effect was not limited to cells exposed at the time of meiotic entry but was evident in all subsequent waves of meiosis. To determine if the meiotic effects induced by estrogen result from changes to the soma or germline of the testis, we transplanted spermatogonial stem cells from exposed males into the testes of unexposed males. Reduced recombination was evident in meiocytes derived from colonies of transplanted cells. Taken together, our results suggest that brief exogenous estrogenic exposure causes subtle changes to the stem cell pool that result in permanent alterations in spermatogenesis (i.e., reduced recombination in descendent meiocytes) in the adult male.

Author Summary
During the past several decades, the incidence of human male reproductive abnormalities such as hypospadias, undescended testicles, testicular cancer, and low sperm counts has increased. Environmental factors—and in particular, exposure to environmental estrogens—have been implicated as contributing factors and, indeed, developmental exposure to a range of estrogenic chemicals induces similar defects in male rodents. Given the wide variety of ‘weak’ estrogenic chemicals found in everyday products, understanding how estrogenic exposures affect sperm production has direct human relevance. Here we show that brief exposure of newborn male mice to exogenous estrogen affects the developing spermatogonial stem cells of the testis and this, in turn, permanently alters spermatogenesis in the adult. Specifically, estrogens adversely affect meiotic recombination, a process that is essential for the production of haploid gametes. Subtle changes in the levels of recombination increase the incidence of meiotic errors, resulting in the elimination of cells before they become sperm. Thus, in addition to their other potential effects on the developing brain and reproductive tract, our results suggest that estrogenic exposures can act to reduce sperm production by affecting the spermatogonial stem cell pool of the developing testis.

Hunt's colleagues on the study were Lisa Vrooman, Jon Oatley, Jodi Griswold and Terry Hassold.

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