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bisphenol A |
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CHEBI:33216 |
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A bisphenol that is 4,4'-methanediyldiphenol in which the methylene hydrogens are replaced by two methyl groups. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:47094, CHEBI:22900, CHEBI:31295
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No supplier information found for this compound. |
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Molfile
XML
SDF
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more structures >>
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call loadScript javascripts\jsmol\core\package.js call loadScript javascripts\jsmol\core\core.z.js -- required by ClazzNode call loadScript javascripts\jsmol\J\awtjs2d\WebOutputChannel.js Jmol JavaScript applet jmolApplet0_object__220262662469182__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__220262662469182__) call loadScript javascripts\jsmol\core\corestate.z.js viewerOptions: { "name":"jmolApplet0_object","applet":true,"documentBase":"https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:33216","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__220262662469182__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"220262662469182","bgcolor":"#000" } (C) 2012 Jmol Development Jmol Version: 13.2.7 $Date: 2013-10-01 11:35:15 -0500 (Tue, 01 Oct 2013) $ java.vendor: j2s java.version: 0.0 os.name: j2s Access: ALL memory: 0.0/0.0 processors available: 1 useCommandThread: false appletId:jmolApplet0_object (signed) starting HoverWatcher_1 getValue emulate = null defaults = "Jmol" getValue boxbgcolor = null getValue bgcolor = #000 backgroundColor = "#000" getValue ANIMFRAMECallback = null getValue APPLETREADYCallback = Jmol._readyCallback APPLETREADYCallback = "Jmol._readyCallback" getValue ATOMMOVEDCallback = null getValue CLICKCallback = null getValue ECHOCallback = null getValue ERRORCallback = null getValue EVALCallback = null getValue HOVERCallback = null getValue LOADSTRUCTCallback = null getValue MEASURECallback = null getValue MESSAGECallback = null getValue MINIMIZATIONCallback = null getValue PICKCallback = null getValue RESIZECallback = null getValue SCRIPTCallback = null getValue SYNCCallback = null getValue STRUCTUREMODIFIEDCallback = null getValue doTranslate = null language=en_US getValue popupMenu = null getValue script = null Jmol applet jmolApplet0_object__220262662469182__ ready call loadScript javascripts\jsmol\core\corescript.z.js call loadScript javascripts\jsmol\J\script\FileLoadThread.js starting QueueThread0_2 script 1 started starting HoverWatcher_3 starting HoverWatcher_4 The Resolver thinks Mol 2OH - Ideal conformer RDKit 3D starting HoverWatcher_5 Time for openFile(2OH - Ideal conformer RDKit 3D 33 34 0 0 0 0 0 0 0 0999 V2000 1.7540 -1.1000 4.0360 O 0 0 0 0 0 0 0 0 0 0 0 0 1.7980 -1.0790 2.6760 C 0 0 0 0 0 0 0 0 0 0 0 0 1.5380 -2.2430 1.9520 C 0 0 0 0 0 0 0 0 0 0 0 0 1.5820 -2.2210 0.5580 C 0 0 0 0 0 0 0 0 0 0 0 0 2.1020 0.1060 2.0060 C 0 0 0 0 0 0 0 0 0 0 0 0 2.1450 0.1270 0.6120 C 0 0 0 0 0 0 0 0 0 0 0 0 1.8850 -1.0360 -0.1120 C 0 0 0 0 0 0 0 0 0 0 0 0 1.9310 -1.0130 -1.6030 C 0 0 0 0 0 0 0 0 0 0 0 0 2.2820 0.3850 -2.2490 C 0 0 0 0 0 0 0 0 0 0 0 0 0.5010 -1.3310 -2.1750 C 0 0 0 0 0 0 0 0 0 0 0 0 3.0070 -2.0090 -2.1910 C 0 0 0 0 0 0 0 0 0 0 0 0 4.2930 -1.8020 -1.8230 C 0 0 0 0 0 0 0 0 0 0 0 0 5.2440 -2.6810 -2.3430 C 0 0 0 0 0 0 0 0 0 0 0 0 2.5520 -2.9820 -3.0120 C 0 0 0 0 0 0 0 0 0 0 0 0 3.5030 -3.8610 -3.5320 C 0 0 0 0 0 0 0 0 0 0 0 0 4.8480 -3.7100 -3.1970 C 0 0 0 0 0 0 0 0 0 0 0 0 5.7760 -4.5670 -3.7060 O 0 0 0 0 0 0 0 0 0 0 0 0 1.3480 -1.9250 4.3470 H 0 0 0 0 0 0 0 0 0 0 0 0 1.3010 -3.1690 2.4680 H 0 0 0 0 0 0 0 0 0 0 0 0 1.3780 -3.1330 0.0020 H 0 0 0 0 0 0 0 0 0 0 0 0 2.3040 1.0160 2.5640 H 0 0 0 0 0 0 0 0 0 0 0 0 2.3820 1.0550 0.0980 H 0 0 0 0 0 0 0 0 0 0 0 0 1.5220 1.1320 -1.9920 H 0 0 0 0 0 0 0 0 0 0 0 0 3.2480 0.7570 -1.8890 H 0 0 0 0 0 0 0 0 0 0 0 0 2.3420 0.3500 -3.3440 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.2300 -0.6290 -1.7540 H 0 0 0 0 0 0 0 0 0 0 0 0 0.4310 -1.2530 -3.2670 H 0 0 0 0 0 0 0 0 0 0 0 0 0.1740 -2.3390 -1.8930 H 0 0 0 0 0 0 0 0 0 0 0 0 4.6100 -1.0040 -1.1580 H 0 0 0 0 0 0 0 0 0 0 0 0 6.2900 -2.5580 -2.0790 H 0 0 0 0 0 0 0 0 0 0 0 0 1.5060 -3.1070 -3.2790 H 0 0 0 0 0 0 0 0 0 0 0 0 3.1890 -4.6610 -4.1980 H 0 0 0 0 0 0 0 0 0 0 0 0 6.6710 -4.2350 -3.5320 H 0 0 0 0 0 0 0 0 0 0 0 0 1 2 1 0 1 18 1 0 2 3 2 0 2 5 1 0 3 4 1 0 3 19 1 0 4 7 2 0 4 20 1 0 5 6 2 0 5 21 1 0 6 7 1 0 6 22 1 0 7 8 1 0 8 11 1 0 8 9 1 0 8 10 1 0 9 23 1 0 9 24 1 0 9 25 1 0 10 26 1 0 10 27 1 0 10 28 1 0 11 12 2 0 11 14 1 0 12 13 1 0 12 29 1 0 13 16 2 0 13 30 1 0 14 15 2 0 14 31 1 0 15 16 1 0 15 32 1 0 16 17 1 0 17 33 1 0 M END): 23 ms reading 33 atoms ModelSet: haveSymmetry:false haveUnitcells:false haveFractionalCoord:false 1 model in this collection. Use getProperty "modelInfo" or getProperty "auxiliaryInfo" to inspect them. Default Van der Waals type for model set to Babel 33 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
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Bisphenol A (BPA) is a chemical compound primarily used in the manufacturing of various plastics. It is a colourless solid which is soluble in most common organic solvents, but has very poor solubility in water. BPA is produced on an industrial scale by the condensation reaction of phenol and acetone. Global production in 2022 was estimated to be in the region of 10 million tonnes.
BPA's largest single application is as a co-monomer in the production of polycarbonates, which accounts for 65–70% of all BPA production. The manufacturing of epoxy resins and vinyl ester resins account for 25–30% of BPA use. The remaining 5% is used as a major component of several high-performance plastics, and as a minor additive in PVC, polyurethane, thermal paper, and several other materials. It is not a plasticizer, although it is often wrongly labelled as such.
The health effects of BPA have been the subject of prolonged public and scientific debate. BPA is a xenoestrogen, exhibiting hormone-like properties that mimic the effects of estrogen in the body. Although the effect is very weak, the pervasiveness of BPA-containing materials raises concerns, as exposure is effectively lifelong. Many BPA-containing materials are non-obvious but commonly encountered, and include coatings for the inside of food cans, clothing designs, shop receipts, and dental fillings. BPA has been investigated by public health agencies in many countries, as well as by the World Health Organization.
While normal exposure is below the level currently associated with risk, several jurisdictions have taken steps to reduce exposure on a precautionary basis, in particular by banning BPA from baby bottles. There is some evidence that BPA exposure in infants has decreased as a result of this. BPA-free plastics have also been introduced, which are manufactured using alternative bisphenols such as bisphenol S and bisphenol F, but there is also controversy around whether these are actually safer.
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Read full article at Wikipedia
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InChI=1S/C15H16O2/c1-15(2,11-3-7-13(16)8-4-11)12-5-9-14(17)10-6-12/h3-10,16-17H,1-2H3 |
IISBACLAFKSPIT-UHFFFAOYSA-N |
CC(C)(C1=CC=C(O)C=C1)C1=CC=C(O)C=C1 |
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environmental contaminant
Any minor or unwanted substance introduced into the environment that can have undesired effects.
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xenoestrogen
A synthetic or semi-synthetic compound that has oestrogenic activity.
xenobiotic
A xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
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endocrine disruptor
Any compound that can disrupt the functions of the endocrine (hormone) system
xenoestrogen
A synthetic or semi-synthetic compound that has oestrogenic activity.
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View more via ChEBI Ontology
4,4'-(propane-2,2-diyl)diphenol
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2, 2-Bis(4-hydroxyphenyl)propane
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HMDB
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2,2-Bis(4'-hydroxyphenyl)propane
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HMDB
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2,2-Bis(4-Hydroxyphenyl)propane
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KEGG COMPOUND
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2,2-Bis(p-hydroxyphenyl)propane
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ChemIDplus
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2,2-Di(4-hydroxyphenyl)propane
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ChemIDplus
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2,2-Di(4-phenylol)propane
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ChemIDplus
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4,4'-(1-Methylethane-1,1-diyl)diphenol
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HMDB
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4,4'-(1-Methylethylidene)bisphenol
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ChemIDplus
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4,4'-(Propane-2,2-diyl)diphenol
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HMDB
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4,4'-Bisphenol A
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ChemIDplus
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4,4'-Isopropylidenediphenol
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ChemIDplus
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Bisphenol A
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KEGG COMPOUND
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bisphenol A
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UniProt
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bisphenol-A
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ChEBI
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BPA
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HMDB
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Dianin's compound
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ChEBI
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1107700
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Reaxys Registry Number
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Reaxys
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80-05-7
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CAS Registry Number
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KEGG COMPOUND
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80-05-7
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CAS Registry Number
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NIST Chemistry WebBook
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80-05-7
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CAS Registry Number
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ChemIDplus
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Resnik DB, Elliott KC (2015) Bisphenol A and risk management ethics. Bioethics 29, 182-189 [PubMed:24471646] [show Abstract] It is widely recognized that endocrine disrupting compounds, such as Bisphenol A, pose challenges for traditional paradigms in toxicology, insofar as these substances appear to have a wider range of low-dose effects than previously recognized. These compounds also pose challenges for ethics and policymaking. When a chemical does not have significant low-dose effects, regulators can allow it to be introduced into commerce or the environment, provided that procedures and rules are in place to keep exposures below an acceptable level. This option allows society to maximize the benefits from the use of the chemical while minimizing risks to human health or the environment, and it represents a compromise between competing values. When it is not possible to establish acceptable exposure levels for chemicals that pose significant health or environmental risks, the most reasonable options for risk management may be to enact either partial or complete bans on their use. These options create greater moral conflict than other risk management strategies, leaving policymakers difficult choices between competing values. | Ferreira LL, Couto R, Oliveira PJ (2015) Bisphenol A as epigenetic modulator: setting the stage for carcinogenesis? European journal of clinical investigation 45 Suppl 1, 32-36 [PubMed:25524584] [show Abstract]
BackgroundBisphenol A (BPA) is one of the most widely produced chemicals worldwide and is often used in the production of food and beverage containers. As a result of BPA contact with food, drink and toiletries, its ingestion and absorption by humans has been growing. The industrialization and modern lifestyles brought a constant exposure to several health-disturbing compounds and ushered a new era of chronic diseases. The endocrine disruptor potential of BPA is well known, but the research around its epigenotoxic effects raised further concerns whether chronic exposure to BPA can contribute to chronic human illness, including cancer in hormone-sensitive organs.Materials and methodsFocusing on computerized databases, we reviewed original and review articles which elucidate and link some of the information already available about BPA and related epigenetic alterations.ResultsA number of studies indicate that short-term administration of low or high-doses of BPA may be associated with an increased risk of epigenetic modifications, increasing the risk for carcinogenesis. However, it is clear that more studies considering real daily exposures are essential to define a real tolerable daily intake and to tighten up manufactory regulations.ConclusionIn this review, we highlight some evidences suggesting a relationship between BPA exposure, genotoxic activity and epigenetic modifications, which may prime for carcinogenesis. | Niu Y, Zhang J, Duan H, Wu Y, Shao B (2015) Bisphenol A and nonylphenol in foodstuffs: Chinese dietary exposure from the 2007 total diet study and infant health risk from formulas. Food chemistry 167, 320-325 [PubMed:25148994] [show Abstract] Concentrations of bisphenol A (BPA) and nonylphenol (NP) were measured in food samples from the 2007 Chinese total diet study (TDS). BPA and NP were detected in 72 and 143 of 144 TDS samples, respectively, with concentrations ranging from 20 ng/kg to 267 μg/kg and 30 ng/kg to 1,268 μg/kg, respectively. BPA was highest in Hebei (HB) province for most food groups. NP was much higher in milk than in other foods across all the provinces. Mean exposures to BPA and NP were estimated to be 43 ng/kg bw/day and 520 ng/kg bw/day for a Chinese adult, respectively, well below the tolerable daily intake (TDI). Mean exposure to NP from formula for infants aged 0-6 years ranged from 300 ng/kg bw/day to 17 μg/kg bw/day. For infants aged 0-1 year, intakes ranged from 5 to 17 μg/kg bw/day, which is above the TDI. | Fang F, Chen D, Yu P, Qian W, Zhou J, Liu J, Gao R, Wang J, Xiao H (2015) Effects of Bisphenol A on glucose homeostasis and brain insulin signaling pathways in male mice. General and comparative endocrinology 212, 44-50 [PubMed:25637671] [show Abstract] The potential effects of Bisphenol A (BPA) on peripheral insulin resistance have recently gained more attention, however, its functions on brain insulin resistance are still unknown. The aim of the present study was to investigate the effects of BPA on insulin signaling and glucose transport in mouse brain. The male mice were administrated of 100 μg/kg/day BPA or vehicle for 15 days then challenged with glucose and insulin tolerance tests. The insulin levels were detected with radioimmunoassay (RIA), and the insulin signaling pathways were investigated by Western blot. Our results revealed that BPA significantly increased peripheral plasma insulin levels, and decreased the insulin signals including phosphorylated insulin receptor (p-IR), phosphorylated insulin receptor substrate 1 (p-IRS1), phosphorylated protein kinase B (p-AKT), phosphorylated glycogen synthase kinase 3β (p-GSK3β) and phosphorylated extracellular regulated protein kinases (p-ERK1/2) in the brain, though insulin expression in both hippocampus and profrontal cortex was increased. In parallel, BPA exposure might contribute to glucose transport disturbance in the brain since the expression of glucose transporters were markedly decreased. In conclusion, BPA exposure perturbs the insulin signaling and glucose transport in the brain, therefore, it might be a risk factor for brain insulin resistance. | Vojdani A, Kharrazian D, Mukherjee PS (2015) Elevated levels of antibodies against xenobiotics in a subgroup of healthy subjects. Journal of applied toxicology : JAT 35, 383-397 [PubMed:25042713] [show Abstract] In spite of numerous research efforts, the exact etiology of autoimmune diseases remains largely unknown. Genetics and environmental factors, including xenobiotics, are believed to be involved in the induction of autoimmune disease. Some environmental chemicals, acting as haptens, can bind to a high-molecular-weight carrier protein such as human serum albumin (HSA), causing the immune system to misidentify self-tissue as an invader and launch an immune response against it, leading to autoimmunity. This study aimed to examine the percentage of blood samples from healthy donors in which chemical agents mounted immune challenges and produced antibodies against HSA-bound chemicals. The levels of specific antibodies against 12 different chemicals bound to HSA were measured by ELISA in serum from 400 blood donors. We found that 10% (IgG) and 17% (IgM) of tested individuals showed significant antibody elevation against aflatoxin-HSA adduct. The percentage of elevation against the other 11 chemicals ranged from 8% to 22% (IgG) and 13% to 18% (IgM). Performance of serial dilution and inhibition of the chemical-antibody reaction by specific antigens but not by non-specific antigens were indicative of the specificity of these antibodies. Although we lack information about chemical exposure in the tested individuals, detection of antibodies against various protein adducts may indicate chronic exposure to these chemical haptens in about 20% of the tested individuals. Currently the pathological significance of these antibodies in human blood is still unclear, and this protein adduct formation could be one of the mechanisms by which environmental chemicals induce autoimmune reactivity in a significant percentage of the population. | Liu J, Jin X, Zhao N, Ye X, Ying C (2015) Bisphenol A promotes X-linked inhibitor of apoptosis protein-dependent angiogenesis via G protein-coupled estrogen receptor pathway. Journal of applied toxicology : JAT 35, 1309-1317 [PubMed:25663485] [show Abstract] Bisphenol A (BPA), one of the high-volume chemicals worldwide, has a core structure resembling that of natural estradiol. Recent evidence has demonstrated that exposure to BPA has a relationship with the risk of cancer. The objective of our study is to investigate the mechanisms underlying the pro-angiogenic effects of BPA. We demonstrated that BPA markedly induces endothelial cell proliferation, migration and tube formation by activating endothelial nitric oxide synthase. BPA-induced nitric oxide generation appeared to be associated with the X-linked inhibitor of apoptosis protein (XIAP), which competes with endothelial nitric oxide synthase for caveolin-1. BPA was shown to exert its pro-angiogenic effect by upregulating XIAP expression via G protein-coupled estrogen receptor (ER) activation but not via ERα or ERβ. Our data suggest that 100 nM BPA promote angiogenesis in a G protein-coupled ER-dependent genomic pathway, and provide a novel insight into the potential role of XIAP in mediating the pro-angiogenic effects of BPA in endothelial cells. | Gao H, Yang BJ, Li N, Feng LM, Shi XY, Zhao WH, Liu SJ (2015) Bisphenol A and hormone-associated cancers: current progress and perspectives. Medicine 94, e211 [PubMed:25569640] [show Abstract] Bisphenol A (BPA), a carbon-based synthetic compound, exhibits hormone-like properties and is present ubiquitously in the environment and in human tissues due to its widespread use and biological accumulation. BPA can mimic estrogen to interact with estrogen receptors α and β, leading to changes in cell proliferation, apoptosis, or migration and thereby, contributing to cancer development and progression. At the genetic level, BPA has been shown to be involved in multiple oncogenic signaling pathways, such as the STAT3, MAPK, and PI3K/AKT pathways. Moreover, BPA may also interact with other steroid receptors (such as androgen receptor) and plays a role in prostate cancer development. This review summarizes the current literature regarding human exposure to BPA, the endocrine-disrupting effects of BPA, and the role of BPA in hormone-associated cancers of the breast, ovary, and prostate. | Kuruto-Niwa R, Tateoka Y, Usuki Y, Nozawa R (2007) Measurement of bisphenol A concentrations in human colostrum. Chemosphere 66, 1160-1164 [PubMed:16904728] [show Abstract] Bisphenol A (BPA), an estrogenic endocrine disrupting chemical, has been reported to affect embryos and alter their postnatal development. In the present study, we measured the concentrations of BPA in human colostrum by a competitive enzyme-linked immunosorbent assay (ELISA) with the aim of understanding the present status of BPA burden in human breast milk in Shizuoka, Japan. Human colostral samples were collected from 101 healthy mothers within three days after delivery. The BPA concentrations of colostral samples were estimated by ELISA after the acetonitrile extraction and solid phase extraction column purification. BPA in 101 samples was detected in the concentration range of 1-7 ng ml(-1). The mean concentration of BPA was 3.41+/-0.13 (mean+/-SD) ng ml(-1). This is the first demonstration as to what BPA concentrations are in human colostrum. The BPA concentrations in colostrum were higher than those in blood sera samples obtained from healthy women in a previous study. In our study, there was no significant correlation between the concentrations of BPA in colostrum and the age and parity of mothers. | Masuda S, Terashima Y, Sano A, Kuruto R, Sugiyama Y, Shimoi K, Tanji K, Yoshioka H, Terao Y, Kinae N (2005) Changes in the mutagenic and estrogenic activities of bisphenol A upon treatment with nitrite. Mutation research 585, 137-146 [PubMed:15936980] [show Abstract] Bisphenol A (4,4'isopropylidenediphenol: BPA), an endocrine-disrupting chemical, is contained in food-packaging and can-coating agents as well as in dental sealants. Nitrite is present in vegetables, fish and tap water as an ingredient or contaminant, and also in human saliva. Here, we explored the possible generation of genotoxicity from the reactions of BPA and nitrite under acidic conditions, a situation simulating the stomach. We determined the changes in the mutagenic and estrogenic activities of BPA before and after nitrite treatment. Untreated BPA did not exhibit any mutagenicity. However, the mixture of BPA and sodium nitrite after incubation at pH 3.0 showed strong mutagenic activity toward Salmonella typhimurium strains TA 100 and TA 98 either with or without a metabolic activation system (S9 mix). The clastogenic properties of nitrite-treated and untreated BPA were analyzed by a micronucleus test with male ICR mice. A single gastric intubation of nitrite-treated BPA induced a significantly higher frequency of micronucleated reticulocytes (MNRETs) in mice. The results of analysis of electron spin resonance (ESR) suggest that the expression of the mutagenic activity of nitrite-treated BPA is related to the generation of radicals in the reaction mixture. By applying 1H and 13C NMR, AB-MS and APCI/LC/MS, we identified two compounds 3-nitrobisphenol A and 3,3'-dinitro-bisphenol A. These compounds were synthesized by the reaction of BPA with nitric acid. 3,3'-Dinitro-bisphenol induced a significantly greater frequency of MNRETs in male ICR mice. By applying a green fluorescent protein (GFP)-reporter expression system and an estrogen R(alpha) competitor screening kit, we found that nitrite-treated BPA and 3,3'-dinitro-bisphenol A showed weak estrogenic activity compared to that of untreated BPA. | Kim JY, Jeong HG (2003) Down-regulation of inducible nitric oxide synthase and tumor necrosis factor-alpha expression by bisphenol A via nuclear factor-kappaB inactivation in macrophages. Cancer letters 196, 69-76 [PubMed:12860292] [show Abstract] Bisphenol A [BPA, 2,2bis(4hydroxyphenyl)propane] is reported to have estrogenic activity; however, its influence on cytokine production or immune system function remains unclear. In this study, we investigated the effects of BPA on the production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha), and on the level of inducible nitric oxide synthase (iNOS) and TNF-alpha gene expression in mouse macrophages. BPA alone did not affect NO or TNF-alpha production. In contrast, BPA inhibited lipopolysaccharide (LPS)-induced NO and TNF-alpha production, and the levels of iNOS and TNF-alpha mRNA in a dose-dependent manner. Treatment with ICI 182.780, an estrogenreceptor antagonist, inhibited the suppressive effects of BPA. Transient expression and electrophoretic mobility shift assays with NF-kappaB binding sites revealed that BPA reduced the levels of the LPS-induced NF-kappaB transcription factor complex. These results demonstrate that BPA may affect the regulation of the immune system function by reducing NO and TNF-alpha production via the inhibition of NF-kappaB transactivation mediated through the estradiol receptor. | Tohei A, Suda S, Taya K, Hashimoto T, Kogo H (2001) Bisphenol A inhibits testicular functions and increases luteinizing hormone secretion in adult male rats. Experimental biology and medicine (Maywood, N.J.) 226, 216-221 [PubMed:11361040] [show Abstract] Effects of a xenobiotic estrogen, bisphenol A (BPA), on reproductive functions were investigated using adult male rats. BPA was dissolved into sesame oil and injected s.c. every day (1 mg/rat) for 14 days. Animals were killed by decapitation after the final administration of BPA, and the trunk blood, pituitary, and testes were collected. Plasma concentrations of prolactin were dramatically increased and pituitary contents of prolactin were slightly increased in the BPA group compared to the control group. Plasma concentrations of testosterone were decreased and plasma concentrations of LH were increased in BPA-treated rats compared to control rats. Testicular contents of inhibin were decreased in BPA-treated rats compared to control rats, although plasma concentrations of inhibin were not changed after administration of BPA. The testicular response to hCG for progesterone and testosterone release was decreased in BPA-treated rats. Administration of BPA did not change the pituitary response to luteinizing hormone-releasing hormone (LH-RH) in castrated male rats treated with testosterone. Male sexual behavior also was not changed as a result of BPA treatment. These results suggest that BPA directly inhibits testicular functions and the increased level of plasma LH is probably due to a reduction in the negative feedback regulation by testosterone. The testis is probably a more sensitive site for BPA action than the hypothalamus-pituitary axis. | Farabollini F, Porrini S, Dessì-Fulgherit F (1999) Perinatal exposure to the estrogenic pollutant bisphenol A affects behavior in male and female rats. Pharmacology, biochemistry, and behavior 64, 687-694 [PubMed:10593191] [show Abstract] Bisphenol A (BPA) is an environmental estrogen with potentially aversive effects on public health. In rats, we studied the effects of perinatal exposure to BPA on nonsocial behaviors partly influenced by gonadal hormones. BPA was administered orally to one group of mother rats at a concentration within the range of human exposure from 10 days before mating until the weaning of the pups. In a second group, BPA was given at a higher dosage during a critical period for brain organization, i.e., from day 14 of gestation until day 6 after birth. The offspring of the treated mothers were tested in the holeboard and the elevated plus-maze at 85 days of age. Various aspects of nonsocial behavior were affected by BPA, differently in males and females, confirming that exposure to a weak environmental estrogen in the period of sexual differentiation of the brain can influence adult behavior. However, contrary to our expectation, a clear masculinization of females was not observed. In general, the factor analysis indicated that in treated males both the motivation to explore and anxiety are reduced, while in females, motor activity and motivation to explore are depressed. Because there were no substantial differences between the two modalities of BPA administration, we suggest that the prolonged treatment with the low dosage compensates for the higher dosage given during a shorter steroid-sensitive period. This may be a cause of concern for public health, given the greater incidence of prolonged exposure of humans to low concentrations released into the environment. |
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