Jump to content

Phytoestrogen

From Wikipedia, the free encyclopedia

A phytoestrogen is a plant-derived xenoestrogen (a type of estrogen produced by organisms other than humans) not generated within the endocrine 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 to estradiol (17-β-estradiol), have the ability to cause estrogenic or antiestrogenic effects.[2] Phytoestrogens are not essential nutrients because their absence from the diet does not cause a disease, nor are they known to participate in any normal biological function.[2] Common foods containing phytoestrogens are soy protein, beans, oats, barley, rice, coffee, apples, carrots (see Food Sources section below for bigger list).

Its name comes from the Greek phyto ("plant") and estrogen, the hormone which gives fertility to female mammals. 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 molecular level, of an estrogen and a phytoestrogen allow them to mildly mimic and sometimes act as an antagonist of estrogen.[2] 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 and red clover (phytoestrogen-rich plants) had adverse effects on the fecundity 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 substituted natural phenolic compounds: the coumestans, prenylflavonoids and isoflavones are three of the most active in estrogenic effects in this class.[1] The best-researched are isoflavones, which are commonly found in soy and red 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 of Fusarium, 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 to estrogen receptors (ER).[14] There are two variants of the estrogen receptor, alpha (ER-α) and beta (ER-β) and many phytoestrogens display somewhat higher affinity 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 transactivate peroxisome 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 of genistein are determined by the balance among these pleiotrophic actions.[15][16][17]

Affinities of estrogen receptor ligands for the ERα and ERβ
Ligand Other names Relative binding affinities (RBA, %)a Absolute binding affinities (Ki, nM)a Action
ERα ERβ ERα ERβ
Estradiol E2; 17β-Estradiol 100 100 0.115 (0.04–0.24) 0.15 (0.10–2.08) Estrogen
Estrone E1; 17-Ketoestradiol 16.39 (0.7–60) 6.5 (1.36–52) 0.445 (0.3–1.01) 1.75 (0.35–9.24) Estrogen
Estriol E3; 16α-OH-17β-E2 12.65 (4.03–56) 26 (14.0–44.6) 0.45 (0.35–1.4) 0.7 (0.63–0.7) Estrogen
Estetrol E4; 15α,16α-Di-OH-17β-E2 4.0 3.0 4.9 19 Estrogen
Alfatradiol 17α-Estradiol 20.5 (7–80.1) 8.195 (2–42) 0.2–0.52 0.43–1.2 Metabolite
16-Epiestriol 16β-Hydroxy-17β-estradiol 7.795 (4.94–63) 50 ? ? Metabolite
17-Epiestriol 16α-Hydroxy-17α-estradiol 55.45 (29–103) 79–80 ? ? Metabolite
16,17-Epiestriol 16β-Hydroxy-17α-estradiol 1.0 13 ? ? Metabolite
2-Hydroxyestradiol 2-OH-E2 22 (7–81) 11–35 2.5 1.3 Metabolite
2-Methoxyestradiol 2-MeO-E2 0.0027–2.0 1.0 ? ? Metabolite
4-Hydroxyestradiol 4-OH-E2 13 (8–70) 7–56 1.0 1.9 Metabolite
4-Methoxyestradiol 4-MeO-E2 2.0 1.0 ? ? Metabolite
2-Hydroxyestrone 2-OH-E1 2.0–4.0 0.2–0.4 ? ? Metabolite
2-Methoxyestrone 2-MeO-E1 <0.001–<1 <1 ? ? Metabolite
4-Hydroxyestrone 4-OH-E1 1.0–2.0 1.0 ? ? Metabolite
4-Methoxyestrone 4-MeO-E1 <1 <1 ? ? Metabolite
16α-Hydroxyestrone 16α-OH-E1; 17-Ketoestriol 2.0–6.5 35 ? ? Metabolite
2-Hydroxyestriol 2-OH-E3 2.0 1.0 ? ? Metabolite
4-Methoxyestriol 4-MeO-E3 1.0 1.0 ? ? Metabolite
Estradiol sulfate E2S; Estradiol 3-sulfate <1 <1 ? ? Metabolite
Estradiol disulfate Estradiol 3,17β-disulfate 0.0004 ? ? ? Metabolite
Estradiol 3-glucuronide E2-3G 0.0079 ? ? ? Metabolite
Estradiol 17β-glucuronide E2-17G 0.0015 ? ? ? Metabolite
Estradiol 3-gluc. 17β-sulfate E2-3G-17S 0.0001 ? ? ? Metabolite
Estrone sulfate E1S; Estrone 3-sulfate <1 <1 >10 >10 Metabolite
Estradiol benzoate EB; Estradiol 3-benzoate 10 ? ? ? Estrogen
Estradiol 17β-benzoate E2-17B 11.3 32.6 ? ? Estrogen
Estrone methyl ether Estrone 3-methyl ether 0.145 ? ? ? Estrogen
ent-Estradiol 1-Estradiol 1.31–12.34 9.44–80.07 ? ? Estrogen
Equilin 7-Dehydroestrone 13 (4.0–28.9) 13.0–49 0.79 0.36 Estrogen
Equilenin 6,8-Didehydroestrone 2.0–15 7.0–20 0.64 0.62 Estrogen
17β-Dihydroequilin 7-Dehydro-17β-estradiol 7.9–113 7.9–108 0.09 0.17 Estrogen
17α-Dihydroequilin 7-Dehydro-17α-estradiol 18.6 (18–41) 14–32 0.24 0.57 Estrogen
17β-Dihydroequilenin 6,8-Didehydro-17β-estradiol 35–68 90–100 0.15 0.20 Estrogen
17α-Dihydroequilenin 6,8-Didehydro-17α-estradiol 20 49 0.50 0.37 Estrogen
Δ8-Estradiol 8,9-Dehydro-17β-estradiol 68 72 0.15 0.25 Estrogen
Δ8-Estrone 8,9-Dehydroestrone 19 32 0.52 0.57 Estrogen
Ethinylestradiol EE; 17α-Ethynyl-17β-E2 120.9 (68.8–480) 44.4 (2.0–144) 0.02–0.05 0.29–0.81 Estrogen
Mestranol EE 3-methyl ether ? 2.5 ? ? Estrogen
Moxestrol RU-2858; 11β-Methoxy-EE 35–43 5–20 0.5 2.6 Estrogen
Methylestradiol 17α-Methyl-17β-estradiol 70 44 ? ? Estrogen
Diethylstilbestrol DES; Stilbestrol 129.5 (89.1–468) 219.63 (61.2–295) 0.04 0.05 Estrogen
Hexestrol Dihydrodiethylstilbestrol 153.6 (31–302) 60–234 0.06 0.06 Estrogen
Dienestrol Dehydrostilbestrol 37 (20.4–223) 56–404 0.05 0.03 Estrogen
Benzestrol (B2) – 114 ? ? ? Estrogen
Chlorotrianisene TACE 1.74 ? 15.30 ? Estrogen
Triphenylethylene TPE 0.074 ? ? ? Estrogen
Triphenylbromoethylene TPBE 2.69 ? ? ? Estrogen
Tamoxifen ICI-46,474 3 (0.1–47) 3.33 (0.28–6) 3.4–9.69 2.5 SERM
Afimoxifene 4-Hydroxytamoxifen; 4-OHT 100.1 (1.7–257) 10 (0.98–339) 2.3 (0.1–3.61) 0.04–4.8 SERM
Toremifene 4-Chlorotamoxifen; 4-CT ? ? 7.14–20.3 15.4 SERM
Clomifene MRL-41 25 (19.2–37.2) 12 0.9 1.2 SERM
Cyclofenil F-6066; Sexovid 151–152 243 ? ? SERM
Nafoxidine U-11,000A 30.9–44 16 0.3 0.8 SERM
Raloxifene – 41.2 (7.8–69) 5.34 (0.54–16) 0.188–0.52 20.2 SERM
Arzoxifene LY-353,381 ? ? 0.179 ? SERM
Lasofoxifene CP-336,156 10.2–166 19.0 0.229 ? SERM
Ormeloxifene Centchroman ? ? 0.313 ? SERM
Levormeloxifene 6720-CDRI; NNC-460,020 1.55 1.88 ? ? SERM
Ospemifene Deaminohydroxytoremifene 0.82–2.63 0.59–1.22 ? ? SERM
Bazedoxifene – ? ? 0.053 ? SERM
Etacstil GW-5638 4.30 11.5 ? ? SERM
ICI-164,384 – 63.5 (3.70–97.7) 166 0.2 0.08 Antiestrogen
Fulvestrant ICI-182,780 43.5 (9.4–325) 21.65 (2.05–40.5) 0.42 1.3 Antiestrogen
Propylpyrazoletriol PPT 49 (10.0–89.1) 0.12 0.40 92.8 ERα agonist
16α-LE2 16α-Lactone-17β-estradiol 14.6–57 0.089 0.27 131 ERα agonist
16α-Iodo-E2 16α-Iodo-17β-estradiol 30.2 2.30 ? ? ERα agonist
Methylpiperidinopyrazole MPP 11 0.05 ? ? ERα antagonist
Diarylpropionitrile DPN 0.12–0.25 6.6–18 32.4 1.7 ERβ agonist
8β-VE2 8β-Vinyl-17β-estradiol 0.35 22.0–83 12.9 0.50 ERβ agonist
Prinaberel ERB-041; WAY-202,041 0.27 67–72 ? ? ERβ agonist
ERB-196 WAY-202,196 ? 180 ? ? ERβ agonist
Erteberel SERBA-1; LY-500,307 ? ? 2.68 0.19 ERβ agonist
SERBA-2 – ? ? 14.5 1.54 ERβ agonist
Coumestrol – 9.225 (0.0117–94) 64.125 (0.41–185) 0.14–80.0 0.07–27.0 Xenoestrogen
Genistein – 0.445 (0.0012–16) 33.42 (0.86–87) 2.6–126 0.3–12.8 Xenoestrogen
Equol – 0.2–0.287 0.85 (0.10–2.85) ? ? Xenoestrogen
Daidzein – 0.07 (0.0018–9.3) 0.7865 (0.04–17.1) 2.0 85.3 Xenoestrogen
Biochanin A – 0.04 (0.022–0.15) 0.6225 (0.010–1.2) 174 8.9 Xenoestrogen
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-Prenylnaringenin 8-PN 4.4 ? ? ? Xenoestrogen
Quercetin – <0.001–0.01 0.002–0.040 ? ? 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
Zeranol α-Zearalanol 48–111 ? ? ? Xenoestrogen
Taleranol β-Zearalanol 16 (13–17.8) 14 0.8 0.9 Xenoestrogen
Zearalenone ZEN 7.68 (2.04–28) 9.45 (2.43–31.5) ? ? Xenoestrogen
Zearalanone ZAN 0.51 ? ? ? Xenoestrogen
Bisphenol A BPA 0.0315 (0.008–1.0) 0.135 (0.002–4.23) 195 35 Xenoestrogen
Endosulfan EDS <0.001–<0.01 <0.01 ? ? Xenoestrogen
Kepone Chlordecone 0.0069–0.2 ? ? ? Xenoestrogen
o,p'-DDT – 0.0073–0.4 ? ? ? Xenoestrogen
p,p'-DDT – 0.03 ? ? ? Xenoestrogen
Methoxychlor p,p'-Dimethoxy-DDT 0.01 (<0.001–0.02) 0.01–0.13 ? ? Xenoestrogen
HPTE Hydroxychlor; p,p'-OH-DDT 1.2–1.7 ? ? ? Xenoestrogen
Testosterone T; 4-Androstenolone <0.0001–<0.01 <0.002–0.040 >5000 >5000 Androgen
Dihydrotestosterone DHT; 5α-Androstanolone 0.01 (<0.001–0.05) 0.0059–0.17 221–>5000 73–1688 Androgen
Nandrolone 19-Nortestosterone; 19-NT 0.01 0.23 765 53 Androgen
Dehydroepiandrosterone DHEA; Prasterone 0.038 (<0.001–0.04) 0.019–0.07 245–1053 163–515 Androgen
5-Androstenediol A5; Androstenediol 6 17 3.6 0.9 Androgen
4-Androstenediol – 0.5 0.6 23 19 Androgen
4-Androstenedione A4; Androstenedione <0.01 <0.01 >10000 >10000 Androgen
3α-Androstanediol 3α-Adiol 0.07 0.3 260 48 Androgen
3β-Androstanediol 3β-Adiol 3 7 6 2 Androgen
Androstanedione 5α-Androstanedione <0.01 <0.01 >10000 >10000 Androgen
Etiocholanedione 5β-Androstanedione <0.01 <0.01 >10000 >10000 Androgen
Methyltestosterone 17α-Methyltestosterone <0.0001 ? ? ? Androgen
Ethinyl-3α-androstanediol 17α-Ethynyl-3α-adiol 4.0 <0.07 ? ? Estrogen
Ethinyl-3β-androstanediol 17α-Ethynyl-3β-adiol 50 5.6 ? ? Estrogen
Progesterone P4; 4-Pregnenedione <0.001–0.6 <0.001–0.010 ? ? Progestogen
Norethisterone NET; 17α-Ethynyl-19-NT 0.085 (0.0015–<0.1) 0.1 (0.01–0.3) 152 1084 Progestogen
Norethynodrel 5(10)-Norethisterone 0.5 (0.3–0.7) <0.1–0.22 14 53 Progestogen
Tibolone 7α-Methylnorethynodrel 0.5 (0.45–2.0) 0.2–0.076 ? ? Progestogen
Δ4-Tibolone 7α-Methylnorethisterone 0.069–<0.1 0.027–<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 of in-vitro systems with labeled estradiol and human ERα and ERβ proteins (except the ERβ values from Kuiper et al. (1997), which are rat ERβ). Sources: See template page.

Ecology

[edit]

Phytoestrogens are involved in the synthesis of antifungal benzofurans and phytoalexins, such as medicarpin (common in legumes), and sesquiterpenes, such as capsidiol in tobacco.[19] Soybeans naturally produce isoflavones, and are therefore a dietary source for isoflavones.

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 as food 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 in quail.[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]

According to one study of nine common phytoestrogens in a Western diet, foods with 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. Flax seed and other oilseeds contained the highest total phytoestrogen content, followed by soybeans and tofu.[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. 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.

A more comprehensive list of foods known to contain phytoestrogens includes:

Food content of phytoestrogens is very variable and accurate estimates of intake are therefore difficult and depends on the databases used.[31] Data from the European Prospective Investigation into Cancer and Nutrition found intakes between 1 mg/d in Mediterranean Countries and more than 20 mg/d in the United Kingdom.[32] The high intake in the UK is partly explained by the use of soy in the Chorleywood bread process.[33] An epidemiological study of women in the United States found that the dietary intake of phytoestrogens in healthy post-menopausal Caucasian women is less than one milligram daily.[34]

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 insufficient clinical evidence to determine that phytoestrogens have effects in humans.[35]

Females

[edit]

It is unclear if phytoestrogens have any effect on the cause or prevention of cancer in women.[1][36] Some epidemiological studies have suggested a protective effect against breast cancer.[1][36][37] Additionally, other epidemiological studies found that consumption of soy estrogens is safe for patients with breast cancer, and that it may decrease mortality and recurrence rates.[1][38][39] It remains unclear if phytoestrogens can minimize some of the deleterious effects of low estrogen levels (hypoestrogenism) resulting from oophorectomy, menopause, or other causes.[36] A Cochrane 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, although genistein effects should be further investigated.[40]

Males

[edit]

It is unclear if phytoestrogens have any effect on male sexuality, with conflicting results about the potential effects of isoflavones originating from soy.[1] Some studies showed that isoflavone supplementation had a positive effect on sperm concentration, count, or motility, and increased ejaculate volume.[41][42] Sperm count decline and increasing rate of testicular cancers in the West may be linked to a higher presence of isoflavone phytoestrogens in the diet while in utero, but such a link has not been definitively proven.[43] Furthermore, while there is some evidence that phytoestrogens may affect male fertility, more recent reviews of available studies found no link,[44][45] and instead suggests that healthier diets such as the Mediterranean diet might have a positive effect on male fertility.[45] Neither isoflavones nor soy have been shown to affect male reproductive hormones in healthy individuals.[44][46]

Infant formula

[edit]

Some studies have found that some concentrations of isoflavones may have effects on intestinal cells. At low doses, genistein acted as a weak estrogen and stimulated cell growth; at high doses, it inhibited proliferation and altered cell cycle dynamics. This biphasic response correlates with how genistein is thought to exert its effects.[47] Some reviews express the opinion that more research is needed to answer the question of what effect phytoestrogens may have on infants,[48][49] 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.[50][51][52] The American 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."[53]

Ethnopharmacology

[edit]

In some countries, phytoestrogenic plants have been used for centuries in the treatment of menstrual and menopausal problems, as well as for fertility problems.[54] Plants used that have been shown to contain phytoestrogens include Pueraria mirifica[55] and its close relative kudzu,[56] Angelica,[57] fennel,[28] and anise. In a rigorous study, the use of one such source of phytoestrogen, red clover, has been shown to be safe, but ineffective in relieving menopausal symptoms[58] (black cohosh is also used for menopausal symptoms, but does not contain phytoestrogens[59]).

See also

[edit]

References

[edit]
  1. ^ a b c d e f "Isoflavones". Micronutrient Information Center, Linus Pauling Institute, Oregon State University, Corvallis. October 2016. Retrieved 6 August 2022.
  2. ^ a b c d e f g Yildiz F (2005). Phytoestrogens in Functional Foods. Taylor & Francis Ltd. pp. 3–5, 210–211. ISBN 978-1-57444-508-4.
  3. ^ Hughes CL (Jun 1988). "Phytochemical mimicry of reproductive hormones and modulation of herbivore fertility by phytoestrogens". Environmental Health Perspectives. 78: 171–4. 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. ^ a b Johnston 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): 812–819. doi:10.1007/bf02909525. S2CID 39917693.[permanent 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, Mañes J (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, Bertuzzi T, Nielsen KF (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. ^ a b Turner JV, Agatonovic-Kustrin S, Glass BD (Aug 2007). "Molecular aspects of phytoestrogen selective binding at estrogen receptors". Journal of Pharmaceutical Sciences. 96 (8): 1879–85. doi:10.1002/jps.20987. PMID 17518366.
  15. ^ a b Dang ZC, Lowik C (Jul 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. ^ a b Dang 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. ^ a b Dang ZC, Audinot V, Papapoulos SE, Boutin JA, Löwik CW (Jan 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, Maggi A, Cozzini P (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. ^ a b Korach 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, Browning B (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, Weston RJ, Lawrence SB, Jansen P, Elliott G, Merton DV (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. ^ Thompson LU, Boucher BA, Liu Z, Cotterchio M, Kreiger N (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. ^ van Elswijk DA, Schobel UP, Lansky EP, Irth H, van der Greef J (Jan 2004). "Rapid dereplication of estrogenic compounds in pomegranate (Punica granatum) using on-line biochemical detection coupled to mass spectrometry". Phytochemistry. 65 (2): 233–41. Bibcode:2004PChem..65..233V. doi:10.1016/j.phytochem.2003.07.001. PMID 14732284.
  26. ^ Chadwick LR, Nikolic D, Burdette JE, Overk CR, Bolton JL, van Breemen RB, Fröhlich R, Fong HH, Farnsworth NR, Pauli GF (Dec 2004). "Estrogens and congeners from spent hops (Humulus lupulus)". Journal of Natural Products. 67 (12): 2024–32. doi:10.1021/np049783i. PMC 7418824. PMID 15620245.
  27. ^ Rosenblum ER, Stauber RE, Van Thiel DH, Campbell IM, Gavaler JS (Dec 1993). "Assessment of the estrogenic activity of phytoestrogens isolated from bourbon and beer". Alcoholism: Clinical and Experimental Research. 17 (6): 1207–9. doi:10.1111/j.1530-0277.1993.tb05230.x. PMID 8116832.
  28. ^ a b Albert-Puleo M (Dec 1980). "Fennel and anise as estrogenic agents". Journal of Ethnopharmacology. 2 (4): 337–44. doi:10.1016/S0378-8741(80)81015-4. PMID 6999244.
  29. ^ Bacciottini, Lucia; Falchetti, Alberto; Pampaloni, Barbara; Bartolini, Elisa; Carossino, Anna Maria; Brandi, Maria Luisa (2007). "Phytoestrogens: food or drug?". Clinical Cases in Mineral and Bone Metabolism. 4 (2): 123–130. ISSN 1724-8914. PMC 2781234. PMID 22461212.
  30. ^ Ramsey, Tyler; Li, Yin; Yukitomo, Arao (Nov 1, 2019). "Lavender Products Associated With Premature Thelarche and Prepubertal Gynecomastia: Case Reports and Endocrine-Disrupting Chemical Activities". J Clin Endocrinol Metab. 104 (11): 5393–5405. doi:10.1210/jc.2018-01880. PMC 6773459. PMID 31393563.
  31. ^ Kuhnle, Gunter G.C.; Dell’Aquila, Caterina; Runswick, Shirley A.; Bingham, Sheila A. (2008). "Variability of phytoestrogen content in foods from different sources". Food Chemistry. 113 (4): 1184–1187. doi:10.1016/j.foodchem.2008.08.004.
  32. ^ Zamora-Ros, R; Knaze, V; Luján-Barroso, L; Kuhnle, G G C; Mulligan, A A; Touillaud, M; Slimani, N; Romieu, I; Powell, N; Tumino, R; Peeters, P H M; de Magistris, M S; Ricceri, F; Sonestedt, E; Drake, I (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.
  33. ^ Cauvain, Stanley P. (2006). The Chorleywood bread process. Linda S. Young. Boca Raton, FL: CRC Press. ISBN 1-84569-143-1. OCLC 236341936.
  34. ^ de Kleijn MJ, van der Schouw YT, Wilson PW, Adlercreutz H, Mazur W, Grobbee DE, Jacques PF (Jun 2001). "Intake of dietary phytoestrogens is low in postmenopausal women in the United States: the Framingham study(1-4)". The Journal of Nutrition. 131 (6): 1826–32. doi:10.1093/jn/131.6.1826. PMID 11385074.
  35. ^ Domínguez-López, Inés; Yago-Aragón, Maria; Salas-Huetos, Albert; Tresserra-Rimbau, Anna; Hurtado-Barroso, Sara (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.
  36. ^ a b c Bilal I, Chowdhury A, Davidson J, Whitehead S (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.
  37. ^ Ingram D, Sanders K, Kolybaba M, Lopez D (Oct 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.
  38. ^ Shu XO, Zheng Y, Cai H, Gu K, Chen Z, Zheng W, Lu W (Dec 2009). "Soy food intake and breast cancer survival". JAMA. 302 (22): 2437–43. doi:10.1001/jama.2009.1783. PMC 2874068. PMID 19996398.
  39. ^ Fritz H, Seely D, Flower G, Skidmore B, Fernandes R, Vadeboncoeur S, Kennedy D, Cooley K, Wong R, Sagar S, Sabri E, Fergusson D (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.
  40. ^ Lethaby A, Marjoribanks J, Kronenberg F, Roberts H, Eden J, Brown J (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.
  41. ^ Dabrowski WM (2004). Toxins in Food. CRC Press Inc. p. 95. ISBN 978-0-8493-1904-4.
  42. ^ Mitchell JH, Cawood E, Kinniburgh D, Provan A, Collins AR, Irvine DS (Jun 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.
  43. ^ 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.
  44. ^ a b Messina, Mark; Mejia, Sonia Blanco; Cassidy, Aedin; Duncan, Alison; Kurzer, Mindy; Nagato, Chisato; Ronis, Martin; Rowland, Ian; Sievenpiper, John; Barnes, Stephen (2021-03-27). "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.
  45. ^ a b Nassan, Feiby L.; Chavarro, Jorge E.; Tanrikut, Cigdem (2018-09-01). "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.
  46. ^ 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.
  47. ^ Chen AC, Donovan SM (Jun 2004). "Genistein at a concentration present in soy infant formula inhibits Caco-2BBe cell proliferation by causing G2/M cell cycle arrest". The Journal of Nutrition. 134 (6): 1303–8. doi:10.1093/jn/134.6.1303. PMID 15173388.
  48. ^ Miniello VL, Moro GE, Tarantino M, Natile M, Granieri L, Armenio L (Sep 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.
  49. ^ 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.
  50. ^ Strom BL, Schinnar R, Ziegler EE, Barnhart KT, Sammel MD, Macones GA, Stallings VA, Drulis JM, Nelson SE, Hanson SA (Aug 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.
  51. ^ Giampietro PG, Bruno G, Furcolo G, Casati A, Brunetti E, Spadoni GL, Galli E (Feb 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.
  52. ^ 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.
  53. ^ 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.
  54. ^ Muller-Schwarze D (2006). Chemical Ecology of Vertebrates. Cambridge University Press. p. 287. ISBN 978-0-521-36377-8.
  55. ^ Lee YS, Park JS, Cho SD, Son JK, Cherdshewasart W, Kang KS (December 2002). "Requirement of metabolic activation for estrogenic activity of Pueraria mirifica". Journal of Veterinary Science. 3 (4): 273–277. doi:10.4142/jvs.2002.3.4.273. PMID 12819377.
  56. ^ 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.
  57. ^ Brown D, Walton N (1999). Chemicals from plants: Perspectives on plant secondary products. World Scientific Publishing. pp. 21, 141. ISBN 978-981-02-2773-9.
  58. ^ Geller SE, Shulman LP, van Breemen RB, Banuvar S, Zhou Y, Epstein G, Hedayat S, Nikolic D, Krause EC, Piersen CE, Bolton JL, Pauli GF, Farnsworth NR (2009). "Safety and efficacy of black cohosh and red clover for the management of vasomotor symptoms: A randomized controlled trial". Menopause. 16 (6): 1156–1166. doi:10.1097/gme.0b013e3181ace49b. PMC 2783540. PMID 19609225.
  59. ^ Kennelly EJ, Baggett S, Nuntanakorn P, Ososki AL, Mori SA, Duke J, Coleton M, Kronenberg F (Jul 2002). "Analysis of thirteen populations of black cohosh for formononetin". Phytomedicine. 9 (5): 461–467. doi:10.1078/09447110260571733. PMID 12222669. S2CID 24786174.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Phytoestrogen&oldid=1233342281"