Breast Growth For Genetic Males

could this be the reason WHY bovine ovary works ?

https://en.wikipedia.org/wiki/Adrenodoxin_reductase

NADPH:adrenodoxin oxidoreductase, mitochondrial also known as adrenodoxin reductase is an enzyme that in humans is encoded by the FDXR gene, also known as ADXR. It catalyzes the following reaction:

NADPH + 2 oxidized adrenodoxin —→ 2 reduced adrenodoxin + NADP+ + H+

In both bovine and human genomes there is only a single copy of this gene.[1]

ADXR gene is expressed in all tissues that have mitochondrial P450s. The highest levels of the enzyme is found in the adrenal cortex, granulosa cells of the ovary and leydig cells of the testis that specialize in steroid hormone synthesis.[2] In addition the enzyme is also expressed in the liver, the kidney and the placenta.

Function[edit]

Adrenodoxin reductase is a mitochondrial flavoprotein as it carries a FAD type coenzyme. The enzyme functions as the first electron transfer protein of mitochondrial P450 systems such as P450scc. The FAD coenzyme receives two electrons from NADPH and transfers them one at a time to the electron transfer protein adrenodoxin.[3] Adrenodoxin functions as a mobile shuttle that transfers electrons between ADXR and mitochondrial P450s.[4]

Adrenodoxin reductase has been also called a ferredoxin-NADP+ reductase. But, determination of the sequence and structure of the enzyme revealed that it is completely different from ferredoxin reductase

Ferredoxin—NADP(+) reductase:
'Ferredoxin: NADP+ reductase is the last enzyme in the transfer of electrons during photosynthesis from photosystem I to NADPH.[1] The NADPH is then used as a reducing equivalent in the reactions of the Calvin cycle.[1] Electron cycling from ferredoxin to NADPH only occurs in the light in part because FNR activity is inhibited in the dark.[10] In nonphotosynthetic organisms, the FNR primarily works in reverse to provide reduced ferredoxin for various metabolic pathways. These pathways include nitrogen fixation, terpenoid biosynthesis, steroid metabolism, oxidative stress response, and iron–sulfur protein biogenesis.[6]'

P450scc:
Cholesterol side-chain cleavage enzyme is commonly referred to as P450scc, where "scc" is an acronym for side-chain cleavage. P450scc is a mitochondrial enzyme that catalyzes conversion of cholesterol to pregnenolone. This is the first reaction in the process of steroidogenesis in all mammalian tissues that specialize in the production of various steroid hormones
The highest level of the cholesterol side-chain cleavage system is found in the adrenal cortex and the corpus luteum.[2] The system is also expressed at high levels in steroidogenic theca cells in the ovary, and Leydig cells in the testis.[2] During pregnancy, the placenta also expresses significant levels of this enzyme system.[4] P450scc is also present at much lower levels in several other tissue types, including the brain.[5] In the adrenal cortex, the concentration of adrenodoxin is similar to that of P450scc, but adrenodoxin reductase is expressed at lower levels

In each steroidogenic cell, the expression of the P450scc system proteins is regulated by the trophic hormonal system specific for the cell type.[2] In adrenal cortex cells from zona fasciculata, the expression of the mRNAs encoding all three P450scc proteins is induced by corticotropin (ACTH).[8][17] The trophic hormones increase CYP11A1 gene expression through transcription factors such as steroidogenic factor 1 (SF-1), by the α isoform of activating protein 2 (AP-2) in the human, and many others.[17][18] The production of this enzyme is inhibited notably by the nuclear receptor DAX-1

DAX1 (dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1) is a nuclear receptor protein that in humans is encoded by the NR0B1 gene (nuclear receptor subfamily 0, group B, member 1).[2][3][4] The NR0B1 gene is located on the short (p) arm of the X chromosome between positions 21.3 and 21.2, from base pair 30,082,120 to base pair 30,087,1DAX1 plays an important role in the normal development of several hormone-producing tissues. These tissues include the adrenal glands above each kidney, the pituitary gland and hypothalamus, which are located in the brain, and the male and female reproductive structures (the testes and ovaries). DAX1 controls the activity of certain genes in the cells that form these tissues during embryonic development. Proteins that control the activity of other genes are known as transcription factors. DAX1 also plays a role in regulating hormone production in these tissues after they have been formed.


so , in theory, this may explain the "b.o. point of no return" as it is expressed in the brain as well, the "rewiring" we all talk about? interesting, more research needed, I think..

Cranberry

phytoestrogen

contains: quercertin,Resveratrol

https://en.wikipedia.org/wiki/Cranberry
Cranberry juice is an abundant food source of proanthocyanidins and flavonols[27] and quercetin,[28][29] which are being studied in vitro.[30][31][32][33][34] However, their effectiveness in humans remains unknown, and is limited by poor absorption into cells and rapid excretion.

http://www.livestrong.com/article/21560-...-estrogen/
Resveratrol is a phytoestrogen contained in foods such as grapes, wines, red grape juice, peanuts and some berries, including blueberries, cranberries and bilberries

cancer preventative:
http://www.phytochemicals.info/research/...xtract.php
The extract from cranberry presscake was fractioned to obtain different extracts including a flavonoid rich extract. The different fractions were tested on different tumor cell lines. The flavonoid rich cranberry extract was the most active and inhibited the proliferation of many human tumor lines. The flavonoid rich cranberry extract was most effective against androgen-dependent prostate cells and least effective against estrogen-independent breast cells and androgen-independent prostate cells. Other cancer cell lines, including specific tumor lines of breast, skin, colon, lung and brain, showed intermediate reaction to the cranberry extract. Because the flavonoid rich cranberry extract had similar effect on estrogen-dependent M-C7 breast cells as well as estrogen-independent MDA-MB-435 breast cells the action of extract was not related to any anti-estrogenic action. It is not known which specific flavonoids are responsible for the inhibition of proliferation. Other studies have shown that the flavonoids epigallocatechin gallate(egcg), catechin and epicatechin. The flavonols quercetin, myricetin and resveratrol may also contribute to the anti-proliferation action of the cranberry extract.
http://jn.nutrition.org/content/137/1/186S.full

interesting find:

gigantomastia, macromastia:

one possible cause , besides sensitivity to IGF,Progesterone and Estrogen, is a reaction to D-pencillamine

https://rarediseases.info.nih.gov/gard/9...esources/1
Gigantomastia has been noted as a side effect of treatment with certain medications like D-pencillamine

STUDY MENTHOL ON TRANSDERMAL ABSORPTION OF KETOCONAZOLE

menthol increases absorbtion rate of ketoconazole through skin.
http://en.cnki.com.cn/Article_en/CJFDTOT...001013.htm

OBJECTIVE:To observe the effects of menthol affecting the transdermal anount of Ketoconazole.METHODS:A simple cell was used as experiment apparatus.The Ketoconazole concentration was determined by multi wavelength areal integral UV spectrophotometry.RESULTS:The result showed that menthol helped enhance the skin permeation of Ketoconazole significantly(P0 01).At 3% menthol,the transdermal absorption rate of Ketoconazole in 24 hours increased by about 2.16 time.CONCLUSION:Menthol was able to enhance the transdermal absorption of Ketoconazole.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401672/
The present work focused on the formulation of KTZ transfersomes and the effect of natural permeation enhancers such as Eucalyptus oil, Turpentine oil, and Peppermint oil on the prepared KTZ transfersomes. Developments in the transdermal delivery of drugs offer a potential solution to improvement in the penetration of antifungal agents into the skin. One such approach has been the application of essential oils, such as eucalyptus oil, Peppermint oil, and Turpentine oil.[5] Eucalyptus oil is an effective skin penetration enhancer and it contains 1,8-cineole, a monoterpene cyclic ether which can enhance penetration of both lipophilic and hydrophilic compounds.[6–9] Turpentine oil and Peppermint oil also acts as a penetration enhancer. They increase the penetration of drugs when applied on the skin to give a faster onset of action. Here, an attempt has been made to incorporate both the mechanisms of transfersomes and permeation enhancers.

http://www.jdsjournal.com/article/S0923-...0/fulltext
Reversal of androgenetic alopecia by topical ketoconzole: Relevance of anti-androgenic activity
Ketoconazole (KCZ), an imidazole anti-fungal agent, is known to be effective for the treatment of seborrheic dermatitis and dandruff. In addition, 2% KCZ shampoo was found to improve hair density and the size and proportion of anagen follicles in androgenetic alopecia (AGA) [1] and, in combination with finasteride, to have an additive effect for AGA [2]. Recently, it has been reported that topical application of KCZ stimulates hair growth in C3H/HeN mice [3]. However, whether topical KCZ is effective enough to improve the clinical appearance of AGA is not yet clear.


wonder if menthol will also enhance the absorbtion of Bovine Ovary Vodka? ..hmmm

menthol
https://en.wikipedia.org/wiki/Menthol
Some studies show that menthol acts as GABAA receptor positive allosteric modulator and increases GABAergic transmission in PAG neurons.[5] Menthol also shares anaesthetic properties similar to propofol, by modulating same sites of GABAA receptor.[6]
GABAA_receptor_positive_allosteric_modulator:
In pharmacology, GABAA receptor positive allosteric modulators are positive allosteric modulator (PAM) molecules that increase the activity of the GABAA receptor protein in the vertebrate central nervous system. Unlike GABAA receptor agonists, GABAA PAMs do not bind at the same active site as the γ-Aminobutyric acid (GABA) neurotransmitter molecule: PAMs affect the receptor by binding at a different site on the protein. This is called allosteric modulation

GABA is a major inhibitory neurotransmitter in the Central nervous system. Upon binding, it triggers the GABAA receptor to open its chloride channel to allow chlorine ions into the neuron, making the cell hyperpolarized and less likely to fire. GABAA PAMs bind to a different site and increase the effect of GABA by making the channel open more frequently or for longer when GABA binds. However, they do not have an effect if GABA or another agonist is not present.

In psychopharmacology, GABAA receptor PAMs used as drugs have mainly sedative and anxiolytic effects. Examples of GABAA PAMs include alcohol (ethanol), benzodiazepines such as diazepam (Valium) and alprazolam (Xanax), Z-drugs such as zolpidem (Ambien), and the barbiturate drugs.

Biosynthesis of Neurosteroids[edit]

Neurosteroids are synthesized in the central nervous system (CNS) and the peripheral nervous system (PNS) from cholesterol and steroidal precursors that are imported from the peripheral sources. These sources include 3β-hydroxy-Δ5 derivatives, such as pregnenolone (PREG) and dehydroepiandrosterone (DHEA), their sulfates, and reduced metabolites such as the tetrahydro derivative of progesterone 3α-hydroxy-5α-pregnane-20-one (3α,5α-THPROG). After the local synthesis or from metabolism of adrenal of gonadal steroids many neurosteroids accumulate in the brain.[26][27]

interesting, so in theory, since Menthol absorbs alcohol trandermaly, then perhaps the Bovine ovary Vodka , or even a PM lotion or cream will accelerate in effect as theorized in the GABAA PAMs...

http://www.ncbi.nlm.nih.gov/pubmed/23346663

Green tea in dermatology.

Abstract

The purpose of this brief review is to summarize all in vitro, in vivo, and controlled clinical trials on green tea preparations and their uses in dermatology. An extensive literature search was carried out to identify in vivo and in vitro studies as well as clinical trials. Twenty studies were assessed and the results suggest that oral administration of green tea can be effective in the scavenging of free radicals, cancer prevention, hair loss, and skin aging plus protection against the adverse effects associated with psoralen-UV-A therapy. Topical application of green tea extract should be potentially effective for atopic dermatitis, acne vulgaris, rosacea, androgenetic alopecia, hirsutism, keloids, genital warts, cutaneous leishmaniasis, and candidiosis. There are promising results with the use of green tea for several dermatologic conditions; however, the efficacy of oral and topical green tea has not always been confirmed

green tea extract is in the copper peptide solution I have recently purchased.

Galactose Weight loss ?
https://en.wikipedia.org/wiki/Galactose
Galactose (galacto- + -ose, "milk sugar"), sometimes abbreviated Gal, is a monosaccharide sugar that is less sweet than glucose and fructose. It is a C-4 epimer of glucose.

Galactan is a polymeric form of galactose found in hemicellulose. Galactan can be converted to galactose by hydrolysis.
In the human body, glucose is changed into galactose via hexoneogenesis to enable the mammary glands to secrete lactose. However, most lactose in breast milk is synthesized from galactose taken up from the blood, and only 35±6% is made from galactose from de novo synthesis. [4] Glycerol also contributes some to the mammary galactose production.[5]

here is where it gets interesting:
Galactose promotes fat mobilization in obese lactating and nonlactating women.
http://www.ncbi.nlm.nih.gov/pubmed/21123462
Seven healthy, obese, exclusively breastfeeding women and 7 healthy, obese, nonlactating women were studied on 2 occasions according to a randomized, crossover, single-blinded design. Subjects received drinks providing ≈70% of the daily estimated energy requirement, of which 60% was either glucose or galactose. The primary outcomes were the rate of appearance (Ra) of glycerol and palmitate, and the secondary outcomes were glucose Ra, milk production, energy expenditure, and substrate oxidation.

RESULTS:

Plasma glucose and insulin concentrations were lower (P < 0.05) and those of glycerol, palmitate, free fatty acids, and triglycerides were higher (P < 0.05) during galactose than during glucose feeding in both nonlactating and lactating women. During galactose feeding, glucose Ra was lower (P < 0.01) and glycerol, palmitate, and free fatty acid Ra were higher (P < 0.01) in both groups. During galactose feeding in all women combined, fat oxidation was higher (P = 0.01) and protein oxidation was lower (P < 0.01). Milk production, energy expenditure, and carbohydrate oxidation were similar between glucose and galactose feeding.

CONCLUSIONS:

Galactose consumption is associated with higher endogenous fat mobilization and oxidation during meal absorption. Long-term studies are required to determine whether galactose as an exclusive carbohydrate source would promote body fat loss in obese subjects

I believe, it is the galactose, that is responsible , as it is shown here , that why women who breast feed their children tend to lose weight, due to the galactose mobilized fat distribution. However, one may apply galactose, and do their brushing of boobs and perhaps migrate the fat to relocate in breast? or perhaps just removing stubborn belly fat while trying to achieve NBE

Sources[edit]

Galactose is found in dairy products, sugar beets, other gums and mucilages. It is also synthesized by the body, where it forms part of glycolipids and glycoproteins in several tissues; and is a by-product from the third-generation ethanol production process (from macroalgae


other concurring /duplicate research:
http://ajcn.nutrition.org/content/93/2/374.long
https://www.researchgate.net/publication...ting_women



BTw. Amazon : Galactose 250g German pharmacy production from Vita World ($49.90+ $5.00 S&H)
it is in powder form, however, it may be used as a topical(maybe).

one other thought struck me... if you can mobilize the fat through galactose, I wonder if using something like Maca, or Volufilline or voluplus will redistribute it at the applied topical site.. since you have it mobilized... interesting notion...new form of body sculpting

Benefits of Activated Charcoal

http://www.natural-holistic-health.com/t...-charcoal/


Activated charcoal powder can do these various things because of its ability to attract other substances to its surface and hold them there. This is called “adsorption” (not absorption). Another one of the benefits of activated charcoal is that it can adsorb thousands of times its own weight in harmful substances. One teaspoonful of it has a surface area of more than 10,000 square feet.

The British medical journal, Lancet, discusses the amazing ability of the human skin to allow transfer of liquids, gases, and even micro-particles through its permeable membrane and pores, by the application of a moist, activated charcoal poultice and compress which actually draw bacteria and poisons through the skin and into the poultice or compress! The article describes the use of activated charcoal compresses to speed the healing of wounds and eliminate their odors. But the activated charcoal poultices must be kept moist and warm for this healing process to occur.



It is one of the best substances in poultices for mushroom poisoning, insect stings, brown recluse spider bites, black widow bites, and various types of snake bites. And we’re still not done listing the benefits of activated charcoal


How to Use an Activated Charcoal Poultice

Activated charcoal poultices that are kept moist and warm actually draw toxins and poisons out through the skin tissue. This is because skin is a permeable membrane, which permits a variety of liquids and gases to enter and exit the body.

Make the poultice just large enough to cover the injured part. The paste may be made by mixing equal parts of flax seed meal or corn starch with the activated charcoal, in a bowl, and then adding just enough hot water to make a moderately thick paste. Then spread the paste over a porous cloth, covering over the top with another layer of that same cloth.

Place the poultice over the area to be treated and cover it with a piece of plastic. Cover or wrap with a cloth, to hold it all in place. Secure by a tie, stretch bandage, or pin.

Apply the activated charcoal poultice for 1 or 2 hours. If applied at bedtime, leave it on overnight. Adsorption takes place almost immediately. When it is removed, wash or gently cleanse the area with cool water. Repeat when needed. Poultices should, at the most, be changed every 6-10 hours. Do not put charcoal directly on the broken skin; because it may cause a tattooing effect, blackening the skin for a period of time.

so in essence, you can do a natural transdermal skin detox. I had seen one product (actually bought it) where it basically does the same thing through the soles of your feet. with the build up of natural environmental toxins, this may be a good thing to do from time to time, to help other nbe products work at peak levels.

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 .

Atrazine, main component- 2, 6-DNT continued.

i am somewhat intrigued with the mutagenic properties of this chemical and would like to see how widespread its effects are, and any other possible causation in the biological effects on mammalian species in particular.

Granted, this is not to be used as it can have cancerous effects on the body, this post, as the previous one, it meant to describe the environmental effects as well as the bioavailabilty. it may give credence to why more and more bio-males are having gender issues.

Atrazine does cross the blood-brain barriers and can effect the hypothalamus, it can also reprogram the hypothalamus to react in a non-cis manner. i apologize if this is a somewhat lengthy and mundane post, however, i feel it is necessary to record it.

https://www.researchgate.net/publication...omet_assay
The higher acidity and
the amount of organic matter dissolved in water, the higher
is the stability of Atrazine herbicide in the aquatic environ-
ment .
read the whole article, it also notes that there is no genotoxic results in humans, however some mutagenic effects have been noted at the chromozonal level and DNA damage in lymphocytes in humans.

it can also cause menstrual irregularities, low hormones in women :
http://www.environmentalhealthnews.org/e...gularities

possible culprit/mutagen activator in the atrazine :
http://onlinelibrary.wiley.com/doi/10.10...2/abstract
This study explores the effect of ATZ treatment on the bioactivation of the promutagen, 2, 6-DNT. (more study to follow on this chemical).

similar to BHT , to note, this supplement may be endocrine disruptor:
Food additive[edit]

BHT is primarily used as an antioxidant food additive. In the United States, it is classified as generally recognized as safe (GRAS) based on a National Cancer Institute study from 1979 in rats and mice.[9] It is approved for use in the U.S. by the Food and Drug Administration: For example, 21 CFR § 137.350(a)(4) allows BHT up to 0.0033% by weight in "enriched rice", while 9 CFR § 381.147(f)(1) allows up to 0.01% in poultry "by fat content". It is permitted in the European Union under E321.[10] It is forbidden as food additive in Japan (since 1958), Romania, Sweden, and Australia.[citation needed] Since the 1970s, BHT has been steadily replaced with BHA.[citation needed] Some food companies have voluntarily eliminated BHT from their products.[citation needed] Others like General Mills and Kellogg's announced in February 2015, following a petition by Vani Hari, that they were going to phase it out.[
Antioxidant[edit]

BHT is also used as an antioxidant in products such as cosmetics, pharmaceuticals, rubber, electrical transformer oil (at 0.35%),[12] and embalming fluid. In the petroleum industry, where BHT is known as the fuel additive AO-29, it is used in hydraulic fluids, turbine and gear oils, and jet fuels.[13] BHT is also used to prevent peroxide formation in diethyl ether and other laboratory chemicals.[14]

Some additive products contain BHT as their primary ingredient, while others contain the chemical merely as a component of their formulation, sometimes alongside butylated hydroxyanisole (BHA).[citation needed]

Health effects[edit]

Debate surrounds the link of BHT to cancer risk, asthma and behavioral issues in children;[15] some studies show a potential to increase and some showing a decreased risk.[16][17][18] There is in vitro indication for endocrine disruption with effect on the testes and thyroid.[19] Because of this uncertainty the consumer group Center for Science in the Public Interest recommend to avoid BHT and puts BHT in its "caution" column.[20] The National Cancer Institute determined in 1979 that it was noncarcinogenic in a mouse model.[9]

BHT is marketed as a health food supplement in capsule form. It has been reported to have anti-viral effects, particularly in use against herpes family viruses, sometimes in combination with L-lysine and vitamin C.[21][22][23][24][25][26][27] This latter use has made it into some of the more popular literature.[28][29][30]

Closely related phenol antioxidants exhibit low toxicity. For example, the LD50 of 2,6-di-tert-butylphenol is greater than 9 g/kg

So, its in our foods, its in our waters..its sold as an antioxidant supplement.. quick search on amazon shows it is readily available as a supplement..it is everywhere!