Teratogenicity and toxicity of the new BPA alternative TMBPF, and BPA, BPS, and BPAF in chick embryonic development.

Bisphenol A (BPA) is a widely known, yet controversial reproductive toxin, capable of inducing reproductive, developmental, and somatic growth defects across species. Due to scientific findings and public concern, companies have developed BPA alternatives remarkably similar to BPA. However, these alternatives have had much less testing and oversight, yet they are already being mass-produced and used across industries from plastics to food-contact coatings.

Cytotoxic and apoptotic data of BPA and BPA alternatives TMBPF, BPAF, and BPS in female adult rat and human stem cells.

Here, we used female adult rat adipose-derived stem cells (rASCs) and human adipose-derived stem cells (hASCs) to compare the toxicities and potencies of several widespread environmental toxins that may be endocrine-disrupting chemicals, including bisphenol A (BPA), and the newer BPA alternatives bisphenol S (BPS), bisphenol AF (BPAF), and tetramethyl bisphenol F (TMBPF). Adult stem cells were cultured to 80% confluency and then exposed to BPA (1 and 10 µM), 17β-estradiol (E2; 10 µM), BPS (1 and 10 µM), BPAF (3 × 10-30 µM), TMBPF (0.01-50 µM), or control media alone (with 0.

BPA, BPAF and TMBPF Alter Adipogenesis and Fat Accumulation in Human Mesenchymal Stem Cells, with Implications for Obesity.

Bisphenol A (BPA) is an endocrine-disrupting chemical used in the production of plastics, and is linked to developmental, reproductive, and metabolic disorders including obesity. Manufacturers have begun using 'BPA-free' alternatives instead of BPA in many consumer products. However, these alternatives have had much less testing and oversight, yet they are already being mass-produced and used across industries from plastics to food-contact coatings.

BPA and BPA alternatives BPS, BPAF, and TMBPF, induce cytotoxicity and apoptosis in rat and human stem cells.

Bisphenol A (BPA) is a ubiquitous industrial chemical found in everyday plastic products and materials. Due to scientific findings on the reproductive, developmental, and cellular defects caused by BPA and heightened public awareness, manufacturers have begun to use new chemicals in place of BPA in "BPA-free" products. These alternatives are chemical analogs of BPA and include dozens of new compounds that have undergone relatively little testing and oversight, including: bisphenol S (BPS), bisphenol AF (BPAF), and the recently developed tetramethyl bisphenol F (TMBPF; the monomer of valPure V70).

Data demonstrating distinct embryonic developmental defects induced by bisphenol a alternatives.

Embryos of (African clawed frog) were exposed to the widespread environmental plasticizers bisphenol AF (BPAF; 0.003-3 μM), bisphenol A (BPA; 1-50 μM), or 17β-estradiol (E2; 10 μM) from just after fertilization through 96 hours of development. The potencies and cellular and morphological effects were compared across chemical treatments and controls.

Links between age at menarche, antral follicle count, and body mass index in African American and European American women.

Objective: To examine the relationships between age at menarche, antral follicle count (AFC), and body mass index (BMI) in a multi-ethnic population of women.

Design: Community-based, cross-sectional study.

Setting: Academic setting.

Bisphenol A, Bisphenol AF, di-n-butyl phthalate, and 17β-estradiol have shared and unique dose-dependent effects on early embryo cleavage divisions and development in Xenopus laevis.

Bisphenol A (BPA), Bisphenol AF (BPAF), and di-n-butyl phthalate (DBP) are widespread compounds used in the production of plastics. We used Xenopus laevis to compare their effects on early embryo cell division and development. Directly after in vitro fertilizations, embryos were exposed to BPA, BPAF, DBP, or 17β-estradiol (E2) for up to 96 h.

Adenosine and catecholamine agonists speed the flagellar beat of mammalian sperm by a non-receptor-mediated mechanism.

Activation of rapid motility apparently is one of the first steps of sperm capacitation and can be studied in vitro. Previously we found that 2-chloro-2'-deoxyadenosine or the catecholamine isoproterenol activates mouse sperm motility in vitro via a pathway mediated by cAMP that requires extracellular Ca2+, the atypical sperm adenylyl cyclase, and sperm-specific protein kinase A. We now show that several other adenosine analogs and catecholamines accelerate the flagellar beat of mouse and human sperm.

Soluble adenylyl cyclase (sAC) is indispensable for sperm function and fertilization.

We previously demonstrated that male mice deficient in the soluble adenylyl cyclase (sAC) are sterile and produce spermatozoa with deficits in progressive motility and are unable to fertilize zona-intact eggs. Here, analyses of sAC(-/-) spermatozoa provide additional insights into the functions linked to cAMP signaling. Adenylyl cyclase activity and cAMP content are greatly diminished in crude preparations of sAC(-/-) spermatozoa and are undetectable after sperm purification.

Signaling pathways for modulation of mouse sperm motility by adenosine and catecholamine agonists.

Capacitation of mammalian sperm, including alterations in flagellar motility, is presumably modulated by chemical signals encountered in the female reproductive tract. This work investigates signaling pathways for adenosine and catecholamine agonists that stimulate sperm kinetic activity. We show that 2-chloro-2'-deoxyadenosine and isoproterenol robustly accelerate flagellar beat frequency with EC50s near 10 and 0.

Identical phenotypes of CatSper1 and CatSper2 null sperm.

Among several candidate Ca(2+) entry channels in sperm, only CatSper1 and CatSper2 are known to have required roles in male fertility. Past work with CatSper1 null sperm indicates that a critical lesion in hyperactivated motility underlies the infertility phenotype and is associated with an absence of depolarization-evoked Ca(2+)entry. Here we show that failure of hyperactivation of CatSper2 null sperm similarly correlates with an absence of depolarization evoked Ca(2+) entry.

A role for galanin-like peptide in the integration of feeding, body weight regulation, and reproduction in the mouse.

Galanin-like peptide (GALP) shares sequence homology with galanin and binds to galanin receptors in vitro. GALP neurons in the arcuate nucleus coexpress leptin receptors, and GALP mRNA expression is up-regulated by leptin. Based on these observations, we postulated that GALP plays a role in mediating leptin's inhibitory effects on food intake (FI) and body weight (BW), as well as its stimulatory effect on the reproductive axis.