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Phytoestrogen

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Plant-derived xenoestrogen

Aphytoestrogen is a plant-derivedxenoestrogen (a type ofestrogen produced by organisms other than humans) not generated within theendocrine system, but consumed by eating plants or manufactured foods.[1] Also called a "dietary estrogen", it is a diverse group of naturally occurring nonsteroidal plant compounds that, because of its structural similarity toestradiol (17-β-estradiol), have the ability to cause bothestrogenic or antiestrogenic effects.[1][2]

Phytoestrogens are not essentialnutrients because their absence from the diet does not cause a disease, nor are they known to participate in any normal biological function.[1][2] Common foods containing phytoestrogens aresoybeans andsoy protein concentrate,miso,tempeh, andtofu.[1] Some soy-basedinfant formulas manufactured with soy protein contain isoflavones.[1]

Its name comes from theGreekphyto ("plant") andestrogen, the hormone which gives fertility tofemale mammals.[1] The word "estrus" (Greek οίστρος) means "sexual desire", and "gene" (Greek γόνο) is "to generate". It has been hypothesized that plants use a phytoestrogen as part of their natural defense against the overpopulation of herbivore animals by controlling female fertility.[3][4]

The similarities, at the molecular level, of anestrogen and a phytoestrogen allow them to mildly mimic and sometimes act as an antagonist of estrogen.[1] Phytoestrogens were first observed in 1926,[2][5] but it was unknown if they could have any effect in human or animal metabolism. In the 1940s and early 1950s, it was noticed that some pastures of subterranean clover andred clover (phytoestrogen-rich plants) had adverse effects on thefecundity of grazing sheep.[2][6][7][8]

Chemical structures of the most common phytoestrogens found in plants (top and middle) compared with estrogen (bottom) found in animals

Structure

[edit]

Phytoestrogens mainly belong to a large group of substitutednatural phenolic compounds: thecoumestans,prenylflavonoids andisoflavones are three of the most active in estrogenic effects in this class.[1] The best-researched are isoflavones, which are commonly found insoy andred clover.Lignans have also been identified as phytoestrogens, although they are not flavonoids.[2]Mycoestrogens have similar structures and effects, but are not components of plants; these are mold metabolites ofFusarium, especially common on cereal grains,[9][10][11] but also occurring elsewhere, e.g. on various forages.[12] Although mycoestrogens are rarely taken into account in discussions about phytoestrogens, these are the compounds that initially generated the interest on the topic.[13]

Mechanism of action

[edit]

Phytoestrogens exert their effects primarily through binding toestrogen receptors (ER).[14] There are two variants of the estrogen receptor, alpha (ER-α) and beta (ER-β) and many phytoestrogens display somewhat higheraffinity for ER-β compared to ER-α.[14]

The key structural elements that enable phytoestrogens to bind with high affinity to estrogen receptors and display estradiol-like effects are:[2]

  • The phenolic ring that is indispensable for binding to estrogen receptor
  • The ring of isoflavones mimicking a ring of estrogens at the receptors binding site
  • Low molecular weight similar to estrogens (MW=272)
  • Distance between two hydroxyl groups at the isoflavones nucleus similar to that occurring in estradiol
  • Optimal hydroxylation pattern

In addition to interaction with ERs, phytoestrogens may also modulate the concentration of endogenous estrogens by binding or inactivating some enzymes, and may affect the bioavailability of sex hormones by depressing or stimulating the synthesis of sex hormone-binding globulin (SHBG).[8]

Emerging evidence shows that some phytoestrogens bind to and transactivateperoxisome proliferator-activated receptors (PPARs).[15][16] In vitro studies show an activation of PPARs at concentrations above 1 μM, which is higher than the activation level of ERs.[17][18] At the concentration below 1 μM, activation of ERs may play a dominant role. At higher concentrations (>1 μM), both ERs and PPARs are activated. Studies have shown that both ERs and PPARs influence each other and therefore induce differential effects in a dose-dependent way. The final biological effects ofgenistein are determined by the balance among these pleiotrophic actions.[15][16][17]

Affinities of estrogen receptor ligands for the ERα and ERβ
LigandOther namesRelative binding affinities (RBA, %)aAbsolute binding affinities (Ki, nM)aAction
ERαERβERαERβ
EstradiolE2; 17β-Estradiol1001000.115 (0.04–0.24)0.15 (0.10–2.08)Estrogen
EstroneE1; 17-Ketoestradiol16.39 (0.7–60)6.5 (1.36–52)0.445 (0.3–1.01)1.75 (0.35–9.24)Estrogen
EstriolE3; 16α-OH-17β-E212.65 (4.03–56)26 (14.0–44.6)0.45 (0.35–1.4)0.7 (0.63–0.7)Estrogen
EstetrolE4; 15α,16α-Di-OH-17β-E24.03.04.919Estrogen
Alfatradiol17α-Estradiol20.5 (7–80.1)8.195 (2–42)0.2–0.520.43–1.2Metabolite
16-Epiestriol16β-Hydroxy-17β-estradiol7.795 (4.94–63)50??Metabolite
17-Epiestriol16α-Hydroxy-17α-estradiol55.45 (29–103)79–80??Metabolite
16,17-Epiestriol16β-Hydroxy-17α-estradiol1.013??Metabolite
2-Hydroxyestradiol2-OH-E222 (7–81)11–352.51.3Metabolite
2-Methoxyestradiol2-MeO-E20.0027–2.01.0??Metabolite
4-Hydroxyestradiol4-OH-E213 (8–70)7–561.01.9Metabolite
4-Methoxyestradiol4-MeO-E22.01.0??Metabolite
2-Hydroxyestrone2-OH-E12.0–4.00.2–0.4??Metabolite
2-Methoxyestrone2-MeO-E1<0.001–<1<1??Metabolite
4-Hydroxyestrone4-OH-E11.0–2.01.0??Metabolite
4-Methoxyestrone4-MeO-E1<1<1??Metabolite
16α-Hydroxyestrone16α-OH-E1; 17-Ketoestriol2.0–6.535??Metabolite
2-Hydroxyestriol2-OH-E32.01.0??Metabolite
4-Methoxyestriol4-MeO-E31.01.0??Metabolite
Estradiol sulfateE2S; Estradiol 3-sulfate<1<1??Metabolite
Estradiol disulfateEstradiol 3,17β-disulfate0.0004???Metabolite
Estradiol 3-glucuronideE2-3G0.0079???Metabolite
Estradiol 17β-glucuronideE2-17G0.0015???Metabolite
Estradiol 3-gluc. 17β-sulfateE2-3G-17S0.0001???Metabolite
Estrone sulfateE1S; Estrone 3-sulfate<1<1>10>10Metabolite
Estradiol benzoateEB; Estradiol 3-benzoate10???Estrogen
Estradiol 17β-benzoateE2-17B11.332.6??Estrogen
Estrone methyl etherEstrone 3-methyl ether0.145???Estrogen
ent-Estradiol1-Estradiol1.31–12.349.44–80.07??Estrogen
Equilin7-Dehydroestrone13 (4.0–28.9)13.0–490.790.36Estrogen
Equilenin6,8-Didehydroestrone2.0–157.0–200.640.62Estrogen
17β-Dihydroequilin7-Dehydro-17β-estradiol7.9–1137.9–1080.090.17Estrogen
17α-Dihydroequilin7-Dehydro-17α-estradiol18.6 (18–41)14–320.240.57Estrogen
17β-Dihydroequilenin6,8-Didehydro-17β-estradiol35–6890–1000.150.20Estrogen
17α-Dihydroequilenin6,8-Didehydro-17α-estradiol20490.500.37Estrogen
Δ8-Estradiol8,9-Dehydro-17β-estradiol68720.150.25Estrogen
Δ8-Estrone8,9-Dehydroestrone19320.520.57Estrogen
EthinylestradiolEE; 17α-Ethynyl-17β-E2120.9 (68.8–480)44.4 (2.0–144)0.02–0.050.29–0.81Estrogen
MestranolEE 3-methyl ether?2.5??Estrogen
MoxestrolRU-2858; 11β-Methoxy-EE35–435–200.52.6Estrogen
Methylestradiol17α-Methyl-17β-estradiol7044??Estrogen
DiethylstilbestrolDES; Stilbestrol129.5 (89.1–468)219.63 (61.2–295)0.040.05Estrogen
HexestrolDihydrodiethylstilbestrol153.6 (31–302)60–2340.060.06Estrogen
DienestrolDehydrostilbestrol37 (20.4–223)56–4040.050.03Estrogen
Benzestrol (B2)–114???Estrogen
ChlorotrianiseneTACE1.74?15.30?Estrogen
TriphenylethyleneTPE0.074???Estrogen
TriphenylbromoethyleneTPBE2.69???Estrogen
TamoxifenICI-46,4743 (0.1–47)3.33 (0.28–6)3.4–9.692.5SERM
Afimoxifene4-Hydroxytamoxifen; 4-OHT100.1 (1.7–257)10 (0.98–339)2.3 (0.1–3.61)0.04–4.8SERM
Toremifene4-Chlorotamoxifen; 4-CT??7.14–20.315.4SERM
ClomifeneMRL-4125 (19.2–37.2)120.91.2SERM
CyclofenilF-6066; Sexovid151–152243??SERM
NafoxidineU-11,000A30.9–44160.30.8SERM
Raloxifene–41.2 (7.8–69)5.34 (0.54–16)0.188–0.5220.2SERM
ArzoxifeneLY-353,381??0.179?SERM
LasofoxifeneCP-336,15610.2–16619.00.229?SERM
OrmeloxifeneCentchroman??0.313?SERM
Levormeloxifene6720-CDRI; NNC-460,0201.551.88??SERM
OspemifeneDeaminohydroxytoremifene0.82–2.630.59–1.22??SERM
Bazedoxifene–??0.053?SERM
EtacstilGW-56384.3011.5??SERM
ICI-164,384–63.5 (3.70–97.7)1660.20.08Antiestrogen
FulvestrantICI-182,78043.5 (9.4–325)21.65 (2.05–40.5)0.421.3Antiestrogen
PropylpyrazoletriolPPT49 (10.0–89.1)0.120.4092.8ERα agonist
16α-LE216α-Lactone-17β-estradiol14.6–570.0890.27131ERα agonist
16α-Iodo-E216α-Iodo-17β-estradiol30.22.30??ERα agonist
MethylpiperidinopyrazoleMPP110.05??ERα antagonist
DiarylpropionitrileDPN0.12–0.256.6–1832.41.7ERβ agonist
8β-VE28β-Vinyl-17β-estradiol0.3522.0–8312.90.50ERβ agonist
PrinaberelERB-041; WAY-202,0410.2767–72??ERβ agonist
ERB-196WAY-202,196?180??ERβ agonist
ErteberelSERBA-1; LY-500,307??2.680.19ERβ agonist
SERBA-2–??14.51.54ERβ agonist
Coumestrol–9.225 (0.0117–94)64.125 (0.41–185)0.14–80.00.07–27.0Xenoestrogen
Genistein–0.445 (0.0012–16)33.42 (0.86–87)2.6–1260.3–12.8Xenoestrogen
Equol–0.2–0.2870.85 (0.10–2.85)??Xenoestrogen
Daidzein–0.07 (0.0018–9.3)0.7865 (0.04–17.1)2.085.3Xenoestrogen
Biochanin A–0.04 (0.022–0.15)0.6225 (0.010–1.2)1748.9Xenoestrogen
Kaempferol–0.07 (0.029–0.10)2.2 (0.002–3.00)??Xenoestrogen
Naringenin–0.0054 (<0.001–0.01)0.15 (0.11–0.33)??Xenoestrogen
8-Prenylnaringenin8-PN4.4???Xenoestrogen
Quercetin–<0.001–0.010.002–0.040??Xenoestrogen
Ipriflavone–<0.01<0.01??Xenoestrogen
Miroestrol–0.39???Xenoestrogen
Deoxymiroestrol–2.0???Xenoestrogen
β-Sitosterol–<0.001–0.0875<0.001–0.016??Xenoestrogen
Resveratrol–<0.001–0.0032???Xenoestrogen
α-Zearalenol–48 (13–52.5)???Xenoestrogen
β-Zearalenol–0.6 (0.032–13)???Xenoestrogen
Zeranolα-Zearalanol48–111???Xenoestrogen
Taleranolβ-Zearalanol16 (13–17.8)140.80.9Xenoestrogen
ZearalenoneZEN7.68 (2.04–28)9.45 (2.43–31.5)??Xenoestrogen
ZearalanoneZAN0.51???Xenoestrogen
Bisphenol ABPA0.0315 (0.008–1.0)0.135 (0.002–4.23)19535Xenoestrogen
EndosulfanEDS<0.001–<0.01<0.01??Xenoestrogen
KeponeChlordecone0.0069–0.2???Xenoestrogen
o,p'-DDT–0.0073–0.4???Xenoestrogen
p,p'-DDT–0.03???Xenoestrogen
Methoxychlorp,p'-Dimethoxy-DDT0.01 (<0.001–0.02)0.01–0.13??Xenoestrogen
HPTEHydroxychlor;p,p'-OH-DDT1.2–1.7???Xenoestrogen
TestosteroneT; 4-Androstenolone<0.0001–<0.01<0.002–0.040>5000>5000Androgen
DihydrotestosteroneDHT; 5α-Androstanolone0.01 (<0.001–0.05)0.0059–0.17221–>500073–1688Androgen
Nandrolone19-Nortestosterone; 19-NT0.010.2376553Androgen
DehydroepiandrosteroneDHEA; Prasterone0.038 (<0.001–0.04)0.019–0.07245–1053163–515Androgen
5-AndrostenediolA5; Androstenediol6173.60.9Androgen
4-Androstenediol–0.50.62319Androgen
4-AndrostenedioneA4; Androstenedione<0.01<0.01>10000>10000Androgen
3α-Androstanediol3α-Adiol0.070.326048Androgen
3β-Androstanediol3β-Adiol3762Androgen
Androstanedione5α-Androstanedione<0.01<0.01>10000>10000Androgen
Etiocholanedione5β-Androstanedione<0.01<0.01>10000>10000Androgen
Methyltestosterone17α-Methyltestosterone<0.0001???Androgen
Ethinyl-3α-androstanediol17α-Ethynyl-3α-adiol4.0<0.07??Estrogen
Ethinyl-3β-androstanediol17α-Ethynyl-3β-adiol505.6??Estrogen
ProgesteroneP4; 4-Pregnenedione<0.001–0.6<0.001–0.010??Progestogen
NorethisteroneNET; 17α-Ethynyl-19-NT0.085 (0.0015–<0.1)0.1 (0.01–0.3)1521084Progestogen
Norethynodrel5(10)-Norethisterone0.5 (0.3–0.7)<0.1–0.221453Progestogen
Tibolone7α-Methylnorethynodrel0.5 (0.45–2.0)0.2–0.076??Progestogen
Δ4-Tibolone7α-Methylnorethisterone0.069–<0.10.027–<0.1??Progestogen
3α-Hydroxytibolone–2.5 (1.06–5.0)0.6–0.8??Progestogen
3β-Hydroxytibolone–1.6 (0.75–1.9)0.070–0.1??Progestogen
Footnotes:a = (1)Binding affinity values are of the format "median (range)" (# (#–#)), "range" (#–#), or "value" (#) depending on the values available. The full sets of values within the ranges can be found in the Wiki code. (2) Binding affinities were determined via displacement studies in a variety ofin-vitro systems withlabeled estradiol and humanERα andERβ proteins (except the ERβ values from Kuiper et al. (1997), which are rat ERβ).Sources: See template page.

Ecology

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Phytoestrogens are involved in the synthesis of antifungalbenzofurans andphytoalexins, such asmedicarpin (common inlegumes), andsesquiterpenes, such ascapsidiol in tobacco.[19] Soybeans naturally produce isoflavones, and are therefore a dietary source for isoflavones.[1]

Phytoestrogens are ancient naturally occurring substances, and as dietary phytochemicals they are considered to have coevolved with mammals. In the human diet, phytoestrogens are not the only source of exogenous estrogens.Xenoestrogens (novel, man-made), are found asfood additives[20] and ingredients, and also in cosmetics, plastics, and insecticides. Environmentally, they have similar effects as phytoestrogens, making it difficult to clearly separate the action of these two kind of agents in studies.[21]

Avian studies

[edit]

The consumption of plants with unusual content of phytoestrogens, under drought conditions, has been shown to decrease fertility inquail.[22]Parrot food as available in nature has shown only weak estrogenic activity. Studies have been conducted on screening methods for environmental estrogens present in manufactured supplementary food, with the purpose of aiding reproduction of endangered species.[23]

Food sources

[edit]

Soy-based food products, such as soybeans, miso, tempeh, tofu, meatlesssoy burgers, and soy protein infant foods contain the highest amounts of isoflavones.[1]

According to a 2006 study of nine common phytoestrogens in Canadian foods, the highest relative phytoestrogen content were nuts and oilseeds, followed by soy products, cereals and breads,legumes, meat products, and other processed foods that may contain soy, vegetables, fruits, alcoholic, and nonalcoholic beverages.[24] The highest concentrations of isoflavones are found in soybeans and soybean products followed by legumes, whereas lignans are the primary source of phytoestrogens found in nuts and oilseeds (e.g. flax) and also found in cereals, legumes, fruits and vegetables.[24] Phytoestrogen content varies in different foods, and may vary significantly within the same group of foods (e.g. soy beverages, tofu) depending on processing mechanisms and type of soybean used. Legumes (in particular soybeans), whole grain cereals, and some seeds are high in phytoestrogens.[24]

Food content of phytoestrogens is highly variable, and accurate estimates of intake are therefore difficult and depends on the databases used.[25] Data from theEuropean Prospective Investigation into Cancer and Nutrition found intakes between 1 mg/d inMediterranean Countries and more than 20 mg/d in theUnited Kingdom.[26]

Effects on humans

[edit]

In humans, phytoestrogens are digested in the small intestine, poorly absorbed into the circulatory system, circulate in plasma, and are excreted in the urine. Metabolic influence is different from that of grazing animals due to the differences between ruminant versus monogastric digestive systems.[21]

As of 2020, there is insufficientclinical evidence to determine that phytoestrogens have effects in humans.[27]

Females

[edit]

It is unclear if phytoestrogens have any effect on the cause or prevention of cancer in women.[1][28] Some epidemiological studies have suggested a protective effect against breast cancer.[1][28][29] Additionally, otherepidemiological studies found that consumption of soy estrogens is safe for patients with breast cancer, and that it may decrease mortality and recurrence rates.[1][30][31] It remains unclear if phytoestrogens can minimize some of the deleterious effects of low estrogen levels (hypoestrogenism) resulting fromoophorectomy,menopause, or other causes.[28] ACochrane review of the use of phytoestrogens to relieve the vasomotor symptoms of menopause (hot flashes) stated that there was no conclusive evidence to suggest any benefit to their use, althoughgenistein effects should be further investigated.[32]

Males

[edit]

It remains under study whether phytoestrogens have any effect on male reproductive physiology.[1] Some studies showed that isoflavone supplementation had a positive effect on sperm concentration, count, ormotility, and increased ejaculate volume.[33][34][35] Dietary intake of isoflavones at levels greater than in typical Asian diets does not affect estrogen, testosterone, sperm or semen amounts.[1]

Reviews of available studies found no link of phytoestrogens on male fertility,[36][37] and instead indicate that diets, such as theMediterranean diet, might have a positive effect on male fertility.[37] Neither isoflavones nor soy have been shown to affect male reproductive hormones in healthy individuals.[1][36][38]

Infant formula

[edit]

Infant formulas made with soy protein phytoestrogens are considered safe alternatives to formulas containing dairy ingredients, which may be excluded for infants withgalactosemia and hereditarylactose intolerance.[1]

Some reviews express the opinion that more research is needed to answer the question of what effect phytoestrogens may have on infants,[39][40] but their authors did not find any adverse effects. Studies conclude there are no adverse effects in human growth, development, or reproduction as a result of the consumption of soy-based infant formula compared to conventional cow-milk formula.[1][41][42][43] TheAmerican Academy of Pediatrics states: "although isolated soy protein-based formulas may be used to provide nutrition for normal growth and development, there are few indications for their use in place of cow milk-based formula. These indications include (a) for infants with galactosemia and hereditary lactase deficiency (rare) and (b) in situations in which a vegetarian diet is preferred."[44]

Ethnopharmacology

[edit]

In some countries, phytoestrogenic plants have been used historically in the belief they can treat menstrual, menopausal, and fertility effects.[45] Plants containing phytoestrogens includePueraria mirifica[46] andkudzu.[47]

See also

[edit]

References

[edit]
  1. ^abcdefghijklmnopqr"Isoflavones". Micronutrient Information Center, Linus Pauling Institute, Oregon State University, Corvallis. October 2016. Retrieved6 August 2022.
  2. ^abcdefYildiz F (2005).Phytoestrogens in Functional Foods. Taylor & Francis Ltd. pp. 3–5,210–211.ISBN 978-1-57444-508-4.
  3. ^Hughes CL (June 1988)."Phytochemical mimicry of reproductive hormones and modulation of herbivore fertility by phytoestrogens".Environmental Health Perspectives.78:171–4.Bibcode:1988EnvHP..78..171H.doi:10.1289/ehp.8878171.PMC 1474615.PMID 3203635.
  4. ^Bentley GR, Mascie-Taylor CG (2000).Infertility in the modern world: present and future prospects. Cambridge, UK: Cambridge University Press. pp. 99–100.ISBN 978-0-521-64387-0.
  5. ^Varner JE, Bonner J (1966).Plant Biochemistry. Academic Press.ISBN 978-0-12-114856-0.
  6. ^Bennetts HW, Underwood EJ, Shier FL (1946). "A specific breeding problem of sheep on subterranean clover pastures in Western Australia".Australian Veterinary Journal.22 (1):2–12.doi:10.1111/j.1751-0813.1946.tb15473.x.PMID 21028682.
  7. ^Cunningham IJ, Hogan KG (1954). "Oestrogens in New Zealand pasture plants".N. Z. Vet. J.2 (4):128–134.doi:10.1080/00480169.1954.33166.
  8. ^abJohnston I (2003).Phytochem Functional Foods. CRC Press Inc. pp. 66–68.ISBN 978-0-8493-1754-5.
  9. ^Bennett GA, Shotwell OI (1979)."Zearalenone in cereal grains".J. Amer. Oil. Chemists Soc.56 (9) 812:812–819.doi:10.1007/bf02909525.S2CID 39917693.[dead link]
  10. ^Kuiper-Goodman T, Scott PM, Watanabe H (1987). "Risk assessment of the mycotoxin zearalenone".Regul. Toxicol. Pharmacol.7 (3):253–306.doi:10.1016/0273-2300(87)90037-7.PMID 2961013.
  11. ^Zinedine A, Soriano JM, Moltó JC, et al. (2007). "Review on the toxicity, occurrence, metabolism, detoxification, regulations and intake of zearalenone: an oestrogenic mycotoxin".Food Chem. Toxicol.45 (1):1–18.doi:10.1016/j.fct.2006.07.030.PMID 17045381.
  12. ^Gallo A, Giuberti G, Frisvad JC, et al. (2015)."Review on Mycotoxin Issues in Ruminants: Occurrence in Forages, Effects of Mycotoxin Ingestion on Health Status and Animal Performance and Practical Strategies to Counteract Their Negative Effects".Toxins (Basel).7 (8):3057–111.doi:10.3390/toxins7083057.PMC 4549740.PMID 26274974.
  13. ^Naz RK (1999).Endocrine Disruptors: Effects on Male and Female Reproductive Systems. CRC Press Inc. p. 90.ISBN 978-0-8493-3164-0.
  14. ^abTurner JV, Agatonovic-Kustrin S, Glass BD (August 2007). "Molecular aspects of phytoestrogen selective binding at estrogen receptors".Journal of Pharmaceutical Sciences.96 (8):1879–85.Bibcode:2007JPhmS..96.1879T.doi:10.1002/jps.20987.PMID 17518366.
  15. ^abDang ZC, Lowik C (July 2005). "Dose-dependent effects of phytoestrogens on bone".Trends in Endocrinology and Metabolism.16 (5):207–13.doi:10.1016/j.tem.2005.05.001.PMID 15922618.S2CID 35366615.
  16. ^abDang ZC (May 2009). "Dose-dependent effects of soy phyto-oestrogen genistein on adipocytes: mechanisms of action".Obesity Reviews.10 (3):342–9.doi:10.1111/j.1467-789X.2008.00554.x.PMID 19207876.S2CID 13804244.
  17. ^abDang ZC, Audinot V, Papapoulos SE, et al. (January 2003)."Peroxisome proliferator-activated receptor gamma (PPARgamma ) as a molecular target for the soy phytoestrogen genistein".The Journal of Biological Chemistry.278 (2):962–7.doi:10.1074/jbc.M209483200.PMID 12421816.
  18. ^Dang Z, Löwik CW (May 2004)."The balance between concurrent activation of ERs and PPARs determines daidzein-induced osteogenesis and adipogenesis".Journal of Bone and Mineral Research.19 (5):853–61.doi:10.1359/jbmr.040120.PMID 15068509.
  19. ^Leegood RC, Lea P (1998).Plant Biochemistry and Molecular Biology. John Wiley & Sons. pp. 204,211–213.ISBN 978-0-471-97683-7.
  20. ^Amadasi A, Mozzarelli A, Meda C, et al. (2009)."Identification of xenoestrogens in food additives by an integrated in silico and in vitro approach".Chem. Res. Toxicol.22 (1):52–63.doi:10.1021/tx800048m.PMC 2758355.PMID 19063592.
  21. ^abKorach KS (1998).Reproductive and Developmental Toxicology. Marcel Dekker Ltd. pp. 278–279.ISBN 978-0-8247-9857-4.
  22. ^Leopold AS, Erwin M, Oh J, et al. (January 1976). "Phytoestrogens: adverse effects on reproduction in California quail".Science.191 (4222):98–100.Bibcode:1976Sci...191...98S.doi:10.1126/science.1246602.PMID 1246602.
  23. ^Fidler AE, Zwart S, Pharis RP, et al. (2000). "Screening the foods of an endangered parrot, the kakapo (Strigops habroptilus), for oestrogenic activity using a recombinant yeast bioassay".Reproduction, Fertility, and Development.12 (3–4):191–9.doi:10.1071/RD00041.PMID 11302429.
  24. ^abcThompson LU, Boucher BA, Liu Z, et al. (2006). "Phytoestrogen content of foods consumed in Canada, including isoflavones, lignans, and coumestan".Nutrition and Cancer.54 (2):184–201.doi:10.1207/s15327914nc5402_5.PMID 16898863.S2CID 60328.
  25. ^Kuhnle GG, Dell Aquila C, Runswick SA, et al. (2008)."Variability of phytoestrogen content in foods from different sources".Food Chemistry.113 (4):1184–1187.doi:10.1016/j.foodchem.2008.08.004.
  26. ^Zamora-Ros R, Knaze V, Luján-Barroso L, et al. (2012)."Dietary intakes and food sources of phytoestrogens in the European Prospective Investigation into Cancer and Nutrition (EPIC) 24-hour dietary recall cohort".European Journal of Clinical Nutrition.66 (8):932–941.doi:10.1038/ejcn.2012.36.ISSN 0954-3007.PMID 22510793.S2CID 24241153.
  27. ^Domínguez-López I, Yago-Aragón M, Salas-Huetos A, et al. (August 2020)."Effects of Dietary Phytoestrogens on Hormones throughout a Human Lifespan: A Review".Nutrients.12 (8): 2456.doi:10.3390/nu12082456.ISSN 2072-6643.PMC 7468963.PMID 32824177.
  28. ^abcBilal I, Chowdhury A, Davidson J, et al. (2014)."Phytoestrogens and prevention of breast cancer: The contentious debate".World Journal of Clinical Oncology.5 (4):705–12.doi:10.5306/wjco.v5.i4.705.PMC 4129534.PMID 25302172.
  29. ^Ingram D, Sanders K, Kolybaba M, et al. (October 1997). "Case-control study of phyto-oestrogens and breast cancer".Lancet.350 (9083):990–4.doi:10.1016/S0140-6736(97)01339-1.PMID 9329514.S2CID 12158051.
  30. ^Shu XO, Zheng Y, Cai H, et al. (December 2009)."Soy food intake and breast cancer survival".JAMA.302 (22):2437–43.doi:10.1001/jama.2009.1783.PMC 2874068.PMID 19996398.
  31. ^Fritz H, Seely D, Flower G, et al. (2013)."Soy, red clover, and isoflavones and breast cancer: a systematic review".PLOS ONE.8 (11) e81968.Bibcode:2013PLoSO...881968F.doi:10.1371/journal.pone.0081968.PMC 3842968.PMID 24312387.
  32. ^Lethaby A, Marjoribanks J, Kronenberg F, et al. (2013)."Phytoestrogens for menopausal vasomotor symptoms".The Cochrane Database of Systematic Reviews.2013 (12) CD001395.doi:10.1002/14651858.CD001395.pub4.PMC 10247921.PMID 24323914.
  33. ^Dabrowski WM (2004).Toxins in Food. CRC Press Inc. p. 95.ISBN 978-0-8493-1904-4.
  34. ^Mitchell JH, Cawood E, Kinniburgh D, et al. (June 2001)."Effect of a phytoestrogen food supplement on reproductive health in normal males".Clinical Science.100 (6):613–8.doi:10.1042/CS20000212.PMID 11352776.
  35. ^Patisaul HB, Jefferson W (2010)."The pros and cons of phytoestrogens".Frontiers in Neuroendocrinology.31 (4):400–19.doi:10.1016/j.yfrne.2010.03.003.PMC 3074428.PMID 20347861.
  36. ^abMessina M, Mejia SB, Cassidy A, et al. (27 March 2021)."Neither soyfoods nor isoflavones warrant classification as endocrine disruptors: a technical review of the observational and clinical data".Critical Reviews in Food Science and Nutrition.62 (21):5824–5885.doi:10.1080/10408398.2021.1895054.ISSN 1040-8398.PMID 33775173.S2CID 232408113.
  37. ^abNassan FL, Chavarro JE, Tanrikut C (1 September 2018)."Diet and men's fertility: does diet affect sperm quality?".Fertility and Sterility.110 (4):570–577.doi:10.1016/j.fertnstert.2018.05.025.ISSN 0015-0282.PMID 30196939.S2CID 52179133.
  38. ^Reed KE, Camargo J, Messina M (2020)."Neither soy nor isoflavone intake affects male reproductive hormones: An expanded and updated meta-analysis of clinical studies".Reproductive Toxicology.100:60–67.doi:10.1016/j.reprotox.2020.12.019.PMID 33383165.
  39. ^Miniello VL, Moro GE, Tarantino M, et al. (September 2003). "Soy-based formulas and phyto-oestrogens: a safety profile".Acta Paediatrica.91 (441):93–100.doi:10.1111/j.1651-2227.2003.tb00655.x.PMID 14599051.S2CID 25762109.
  40. ^Chen A, Rogan WJ (2004)."Isoflavones in soy infant formula: a review of evidence for endocrine and other activity in infants".Annual Review of Nutrition.24 (1):33–54.doi:10.1146/annurev.nutr.24.101603.064950.PMID 15189112.
  41. ^Strom BL, Schinnar R, Ziegler EE, et al. (August 2001)."Exposure to soy-based formula in infancy and endocrinological and reproductive outcomes in young adulthood".JAMA.286 (7):807–14.doi:10.1001/jama.286.7.807.PMID 11497534.
  42. ^Giampietro PG, Bruno G, Furcolo G, et al. (February 2004). "Soy protein formulas in children: no hormonal effects in long-term feeding".Journal of Pediatric Endocrinology & Metabolism.17 (2):191–6.doi:10.1515/JPEM.2004.17.2.191.PMID 15055353.S2CID 43304969.
  43. ^Merritt RJ, Jenks BH (May 2004)."Safety of soy-based infant formulas containing isoflavones: the clinical evidence".The Journal of Nutrition.134 (5):1220S–1224S.doi:10.1093/jn/134.5.1220S.PMID 15113975.
  44. ^Bhatia J, Greer F (May 2008)."Use of soy protein-based formulas in infant feeding".Pediatrics.121 (5):1062–8.doi:10.1542/peds.2008-0564.PMID 18450914.S2CID 1482728.
  45. ^Muller-Schwarze D (2006).Chemical Ecology of Vertebrates. Cambridge University Press. p. 287.ISBN 978-0-521-36377-8.
  46. ^Lee YS, Park JS, Cho SD, et al. (December 2002)."Requirement of metabolic activation for estrogenic activity ofPueraria mirifica".Journal of Veterinary Science.3 (4):273–277.doi:10.4142/jvs.2002.3.4.273.PMID 12819377.
  47. ^Delmonte P, Rader JI (2006)."Analysis of isoflavones in foods and dietary supplements".Journal of AOAC International.89 (4):1138–1146.doi:10.1093/jaoac/89.4.1138.PMID 16915857.
Phytoestrogens
Flavanones
Flavones
Prenylflavonoids
Isoflavones
Isoflavanes
Dihydrochalcones
Isoflavenes
Coumestans
Lignans
Flavonolignans
Flavonols
Others
Mycoestrogens
Derivatives
Synthetic
Metalloestrogens
ERTooltip Estrogen receptor
Agonists
Mixed
(SERMsTooltip Selective estrogen receptor modulators)
Antagonists
GPERTooltip G protein-coupled estrogen receptor
Agonists
Antagonists
Unknown
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