[tanysquirrel]

interesting...
Atrazine
{mind you, this is a commonly available and widely used herbicide}
classification:herbicide
http://www.environmentalhealthnews.org/e...ine-health

"But about a decade ago, researchers at University of California, Berkeley, found that low concentrations – the amount expected near farms – caused male tadpoles to turn into female frogs.

Follow-up studies in the wild found that atrazine either turned male tadpoles into females or “demasculinized” them, causing eggs to grow in their testes and rendering them unable to reproduce, said Tyrone Hayes, a UC Berkeley professor of biology who led the research.

The chemical can disrupt hormones and alter male reproductive tissues when an animal is exposed during development. Other impacts include a reduction in size at birth, according to 2005 and 2008 studies of amphibians and fish by University of Texas researchers.

And it’s not just frogs that might be at risk of being feminized – recent research has found that atrazine has similar hormonal effects on salmon, caimans and lab rats
The strongest evidence of a possible human effect is a study comparing men in a rural area of Missouri to men in three urban areas. The Missouri men with higher atrazine exposures were more likely to have poor semen quality, perhaps due to the chemical’s ability to alter sex hormones, according to the study published a decade ago. Similar effects were reported on the sperm of lab animals.

possible activator of the DAX1 (sex reversal gene)??
https://en.wikipedia.org/wiki/Atrazine
A 2002 study by Tyrone Hayes, of the University of California, Berkeley, found that exposure caused male tadpoles to turn into hermaphrodites – frogs with both male and female sexual characteristics.[49] A 2003 EPA review of this study concluded that overcrowding, questionable sample handling techniques, and the failure of the authors to disclose key details including sample sizes, dose-response effects, and the variability of observed effects made it difficult to assess the study's credibility and ecological relevance.[50] According to Hayes in 2004, all of the studies that rejected the hermaphroditism hypothesis were plagued by poor experimental controls and were funded by Syngenta, suggesting conflict of interest.[51] A 2005 Syngenta-funded study, requested by EPA and conducted under EPA guidance and inspection, was unable to reproduce Hayes´ results.[52]

The EPA's Scientific Advisory Panel examined relevant studies and concluded in 2010, "atrazine does not adversely affect amphibian gonadal development based on a review of laboratory and field studies."[10] It recommended proper study design for further investigation. As required by the EPA, Syngenta conducted two experiments under Good Laboratory Practices (GLP) and inspection by EPA and German regulatory authorities, concluding 2009 that "long-term exposure of larval X. laevis to atrazine at concentrations ranging from 0.01 to 100 μg/l does not affect growth, larval development, or sexual differentiation."[53] A 2008 report cited the independent work of researchers in Japan, who were unable to replicate Hayes' work. "The scientists found no hermaphrodite frogs; no increase in aromatase as measured by aromatase mRNA induction; and no increase in vitellogenin, another marker of feminization

http://news.berkeley.edu/2010/03/01/frogs/
Subsequent studies showed that native leopard frogs (Rana pipiens) collected from atrazine-contaminated streams in the Midwest, including from areas up to 1,000 miles from where atrazine is applied, often had eggs in their testes. And many males had lower testosterone levels than normal females and smaller than normal voice boxes, presumably limiting their ability to call mates.
The 10 percent or more that turn from males into females – something not known to occur under natural conditions in amphibians – can successfully mate with male frogs but, because these females are genetically male, all their offspring are male


http://www.pnas.org/content/107/10/4612.full
Atrazine-exposed males were both demasculinized (chemically castrated) and completely feminized as adults. Ten percent of the exposed genetic males developed into functional females that copulated with unexposed males and produced viable eggs. Atrazine-exposed males suffered from depressed testosterone, decreased breeding gland size, demasculinized/feminized laryngeal development, suppressed mating behavior, reduced spermatogenesis, and decreased fertility. These data are consistent with effects of atrazine observed in other vertebrate classes. The present findings exemplify the role that atrazine and other endocrine-disrupting pesticides likely play in global amphibian declines.

In addition to its persistence, mobility, and widespread contamination of water, atrazine is also a concern because several studies have shown that atrazine is a potent endocrine disruptor active in the ppb (parts per billion) range in fish (4, 5), amphibians (6–12), reptiles, and human cell lines (5, 13–15), and at higher doses (ppm) in reptiles (16–18), birds (19), and laboratory rodents (20–28). Atrazine seems to be most potent in amphibians, where it is active at levels as low as 0.1 ppb (6–10). Although a few studies suggest that atrazine has no effect on amphibians under certain laboratory conditions (29, 30), in other studies, atrazine reduces testicular volume; reduces germ cell and Sertoli cell numbers (11); induces hermaphroditism (6, 8, 10); reduces testosterone (10); and induces testicular oogenesis (7–9, 31). Furthermore, atrazine contamination is associated with demasculinization and feminization of amphibians in agricultural areas where atrazine is used (32) and directly correlated with atrazine contamination in the wild (7, 9,

here is a scary thought... :
http://www.livescience.com/6379-frogs-su...aking.html

At least 1,700 genes in the African clawed frog genome are very similar to genes in humans that are associated with specific diseases, such as cancer, asthma, and heart disease. So finding these connections means that experiments on the frogs could help doctors learn more about how to treat those conditions in people.

http://journals.plos.org/plosone/article...ne.0002117
Maintenance of cytochrome p450 aromatase activity, which catalyzes the conversion of androgens to estrogens appears critical for preserving a balanced sex ratio in teleosts. All species lacking sex chromosomes, such as fish [24], are especially sensitive to environmental factors that perturb sex steroid levels. Indeed, increasing estrogen levels in a natural or laboratory setting feminized [25], and greatly altered normal sex ratios in fish [26]. Conversely, treatment with aromatase inhibitors results in gonadal masculinization of female fish [27], [28]. This fact positions aromatase as a potentially useful target to examine the in vivo effects of ATR. In mammals, both ERα and the NR5A nuclear receptor, steroidogenic factor 1 (SF-1) influence expression of the single Cyp19A gene encoding aromatase. In zebrafish (Danio rerio), regulating aromatase expression is more complex because of gene duplication. The gonadal-enriched zcyp19a1 contains an NR5A binding site and is presumably activated by the zebrafish SF-1/LRH-1 orthologs (ff1a, b, c and d) [24], whereas the brain-enriched zcyp19a2 contains an estrogen response element (ERE) and is responsive to estrogens [29], [30] (Fig 1). Both zebrafish aromatase promoters contain CREB binding sites and would therefore be responsive to cAMP signaling. Not surprisingly, studies using several fish species showed upregulation of zcyp19a2, with a notable downregulation of zcyp19a1 after exposure to estrogen, xenoestrogens and other estrogenic chemicals [31], [32]. While a direct link between ATR and zcyp19a1 has not be established, others have shown that at relatively low doses (0.1 µM or 22 µg/L) ATR greatly increases aromatase activity in selective mammalian cell lines [33] and in immortalized sea turtle cells [34].
To determine if ATR might directly affect NR5A receptor activity, and thus account for the increased levels of endogenous zcyp19a1 transcripts, cellular reporter assays were performed. Using JEG3 human placental cells, which contain modest amounts of SF-1, ATR treatment activated the aromatase promoter in a dose-dependent manner (Fig 3A). Similar activation was observed with other SF-1 reporters including those with isolated NR5A binding sites (Fig S1A). However no activation was observed using the parent reporter or with mutant SF-1 binding sites (Fig 3A and S1B) showing that ATR effects depend on DNA binding and receptor occupancy of the promoter, as suggested previously [35], [38]. Activation by ATR was enhanced greatly by overexpression of mSF-1 in JEG3 or HepG2 cells (Fig 3A and 5A), similar to results obtained in human H295R adrenal cortical cells [38]. However, while the response in H295R cells was shown to be selective for SF-1 [35], we find that in all responsive cell lines ATR can also activate hLRH-1 (NR5A2) and its close zebrafish ortholog ff1d, which is expressed in embryonic male gonads [24](Fig 3A). Moreover, knocking-down hLRH-1 in human HepG2 liver cells greatly attenuated ATR activation of the aromatase reporter demonstrating a dependence on this NR5A receptor (Fig S5). Based on these findings, we suggest that all NR5A subfamily receptors will be responsive to ATR.

At activating ATR concentrations (1 µM) we observed a significant and consistent increase in cellular cAMP, albeit at levels much lower than those obtained with forskolin (Fig 4C). Despite these lower levels of cAMP stimulation, forskolin (10 µM), as well as EGF (50 µg/L), activate the aromatase promoter to similar levels observed for ATR (Fig S2). We also asked if ATR might bind directly to SF-1 to either increase DNA binding or act as a ligand.

interesting, if true
if only it was as easy as slathering myself in atrazine (which incidentally , is available on amazon......hahaha)...I wouldn't suggest experimentation .