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  • 1. BPA FREEDo Bisfenol A dosbiberes (e no s!) 2012 Massimiliano Vurro - Antnio Landes

2. Disclaimer [nota:]Com este guia entendemoscolocar disposio, algumas informaes relativas limitao na Europa do Bisfenol A nos biberes para lactantesO guia apenas de caracterinformativo (no tcnico),aconselhamos, portanto, de o usar como tal e deconsultarem sempre os textos de leis oficiais 2012 Massimiliano Vurro - Antnio Landes 3. Classificao ao abrigo doRegulamento 1272/2008 CLPO BPA (Bisfenol A) um composto orgnicoutilizado na produo de plsticos rgidos (policarbonatos) queesto em contactodirecto com os alimentosbisphenol A;(slidos ou lquidos)4,4-isopropylidenediphenolEC#: 201-245-8 CAS#:80-05-7Formula Molecular: C15H16O2Categoria de perigoAviso, indicao de perigosidadeRepr. 2H361f Suspeito de interferir na fertilidadeSTOT SE 3H335 Pode irritar as vias respiratriasEye Dam. 1 H318 Provoca graves leses ocularesSkin Sens. 1 H317 Pode provocar reaces alrgicas cutneas 2012 Massimiliano Vurro - Antnio Landes 4. O alerta em relao ao BPA existe desde 1936 quando seencontrou uma correlao entre asubstncia e osdistrbios que estapode provocar nosistema endcrino 2012 Massimiliano Vurro -Antnio Landes 5. Alguns investigadores j tinham descobertoque o BPA poderia serutilizado como hormnio sinteticoparecido com umestrognio, acreditando que podesse ser til para controlar a gravidezes dificeis 2012 Massimiliano Vurro - Antnio Landes 6. Hoje mais de 150 estudos cientificos em roedoresdemostrariam aperigosidade para o homemdo composto mesmo em doses pequenas 2012 Massimiliano Vurro - Antnio Landes 7. Supplement: The Endocrinology of Endocrine Disrupting ChemicalsLarge Effects from Small Exposures. III. Endocrine Mechanisms Mediating Effects ofBisphenol A at Levels of Human ExposureWade V. Welshons,Susan C. Nagel andFrederick S. vom SaalAuthor AffiliationsDepartment of Biomedical Sciences (W.V.W.), Department of Obstetrics, Gynecology, De acordo comand Womens Health (S.C.N.), and Division of Biological Sciences (F.S.v.S.), Universityof Missouri-Columbia, Columbia, Missouri 65211Address all correspondence and requests for reprints to: Dr. Wade V. Welshons, uma pesquisa deDepartment of Biomedical Sciences, E102 Veterinary Medicine, University ofMissouri-Columbia, Columbia, Missouri 65211-5120. E-mail:WelshonsW@missouri.edu. 2005, o BPAAbstractOver 6 billion pounds per year of the estrogenic monomer bisphenol A (BPA) arepoder ter repercusses noused to manufacture polycarbonate plastic products, in resins lining metal cans, indental sealants, and in blends with other types of plastic products. The ester bondlinking BPA molecules in polycarbonate and resins undergoes hydrolysis, resulting inthe release of free BPA into food, beverages, and the environment, and numerousmonitoring studies now show almost ubiquitous human exposure to biologicallydesenvolvimentocerebral dosactive levels of this chemical. BPA exerts estrogenic effects through the classicalnuclear estrogen receptors, and BPA acts as a selective estrogen receptor modulator.However, BPA also initiates rapid responses via estrogen receptors presumablyassociated with the plasma membrane. Similar to estradiol, BPA causes changes insome cell functions at concentrations between 1 pm and 1 nm, and the mean andbbsmedian range of unconjugated BPA measured by multiple techniques in humanpregnant maternal, fetal, and adult blood and other tissues exceeds these levels. Incontrast to these published findings, BPA manufacturers persist in describing BPA asa weak estrogen and insist there is little concern with human exposure levels. Ourconcern with human exposure to BPA derives from 1) identification of molecularmechanisms mediating effects in human and animal tissues at very low doses, 2) invivo effects in experimental animals caused by low doses within the range of humanexposure, and 3) widespread human exposure to levels of BPA that cause adverseeffects in animals. 2012 Massimiliano Vurro - Antnio Landes 8. Ontogeny of Rapid Estrogen-Mediated Extracellular Signal-Regulated Kinase Signalingin the Rat Cerebellar Cortex: Potent Nongenomic Agonist and Endocrine DisruptingActivity of the Xenoestrogen Bisphenol AAttila Zsarnovszky,Hoa H. Le,Hong-Sheng Wang andScott M. BelcherAuthor AffiliationsDepartment of Pharmacology and Cell Biophysics, University of Cincinnati College ofTambm osMedicine, Cincinnati, Ohio 45267Address all correspondence and requests for reprints to: Scott M. Belcher, Ph.D.,Department of Pharmacology and Cell Biophysics, University of Cincinnati College of investigadores da University of CincinnatiMedicine, 231 Albert Sabin Way, P.O. Box 670575, Cincinnati, Ohio 45267-0575. E-mail:scott.belcher@uc.edu.AbstractIn addition to regulating estrogen receptor-dependent gene expression, 17-estradiol(E2) can directly influence intracellular signaling. In primary cultured cerebellar neurons,E2 was previously shown to regulate growth and oncotic cell death via rapid stimulation(Usa) descobriram queof ERK1/2 signaling. Here we show that ERK1/2 signaling in the cerebellum of neonataland mature rats was rapidly responsive to E2 and during development to the distrbios importantesno tecido cerebral dosenvironmental estrogen bisphenol A (BPA). In vivo dose-response analysis for eachestrogenic compound was performed by brief (6-min) intracerebellar injection, followedby rapid fixation and phosphorylation-state-specific immunohistochemistry toquantitatively characterize changes in activated ERK1/2 (pERK) immunopositive cellnumbers. Beginning on postnatal d 8, E2 significantly influenced the number of pERK-positive cells in a cell-specific manner that was dependent on concentration and age but bbs poderiam sernot sex. In cerebellar granule cells on postnatal d 10, E2 or BPA increased pERK-positivecell numbers at low doses (1012 to 1010 m) and at higher (107 to 106 m) concentrations.provocados at mesmo com doses baixasIntermediate concentrations of either estrogenic compound did not modify basal ERKsignaling. Rapid E2-induced increases in pERK immunoreactivity were specific to theERK1/2 pathway as demonstrated by coinjection of the mitogen-activated, ERK-activating kinase (MEK)1/2 inhibitor U0126. Coadministration of BPA (1012 to 1010 m)with 1010 m E2 dose-dependently inhibited rapid E2-induced ERK1/2 activation indeveloping cerebellar neurons. The ability of BPA to act as a highly potent E2 mimeticand to also disrupt the rapid actions of E2 at very low concentrations during cerebellardevelopment highlights the potential low-dose impact of xenoestrogens on thedeveloping brain. 2012 Massimiliano Vurro - Antnio Landes 9. Perinatal Exposure to Bisphenol-A Alters Peripubertal Mammary Gland Development inMiceMonica Muoz-de-Toro,Caroline M. Markey,Perinaaz R. Wadia,Enrique H. Luque,Beverly S. Rubin,Carlos Sonnenschein andPara Ana Soto daAna M. SotoAuthor AffiliationsDepartment of Anatomy and Cellular Biology (C.M.M., P.R.W., B.S.R., C.S., A.M.S.), TuftsUniversity School of Medicine, Boston, Massachusetts 02111; and Laboratorio deEndocrinologia y Tumores Hormonodependientes (M.M.-d.-T., E.H.L.), Faculty ofBiochemistry and Biological Sciences, Universidad Nacional del Litoral, 3000 Santa Fe,Tufts UniversityArgentinaAddress all correspondence and requests for reprints to: Ana M. Soto, Department ofAnatomy and Cellular Biology, Tufts University School of Medicine, 136 Harrison Avenue,(Usa) il Bisfenol ABoston, Massachusetts 02111. E-mail: ana.soto@tufts.edu.Abstract pode provocarDevelopmental exposure to estrogenic chemicals induces morphological, functional, andbehavioral anomalies associated with reproduction. Humans are exposed to bisphenol-A(BPA), an estrogenic compound that leaches from dental materials and plastic food and cancro da mamae da prstatabeverage containers. The aim of the present study was to determine the effects ofperinatal exposure to low, environmentally relevant doses of BPA [25 and 250 ng BPA/kgbody weight (bw)d] on the peripubertal development of the mammary gland. BPAexposure enhanced the mammary glands sensitivity to estradiol in ovariectomized CD-1mice. In their intact 30-d-old littermates, the area and numbers of terminal end budsrelative to the gland ductal area increased whereas their apoptotic activity decreased. (estudo feito emThere was a positive correlation between ductal length and the age at first proestrus; thatwas reduced as the BPA dose increased, suggesting that BPA exposure slows down ductalinvasion of the stroma. There was also a significant increase of progesterone receptor- roedores)positive ductal epithelial cells that were localized in clusters, suggesting future branchingpoints. Indeed, lateral branching was significantly enhanced at 4 months of age in miceexposed to 25 ng BPA /kg bwd. In conclusion, perinatal exposure to environmentallyrelevant BPA doses results in persistent alterations in mammary gland morphogenesis. Ofspecial concern is the increased terminal end bud density at puberty as well as theincreased number of terminal ends reported previously in adult animals, as these twostructures are the sites at which cancer arises in humans and rodents. 2012 Massimiliano Vurro - Antnio Landes 10. O BPA usa-se para orevestimento interior das conservas de alumnio Dica! Reduzir o uso dealimentos em conserva, emparticular os alimentosquentes ou lquidos.Utilizar recipientes de vidro,cermica ou recipientes em ao inox sem revestimentointerior em plstico 2012 Massimiliano Vurro - Antnio Landes 11. um compostofundamental na produo das tradicionais garrafas de gua em plstico e dealguns cantis de caminhada 2012 Massimiliano Vurro - Antnio Landes 12. um componente das obturaes dentrias 2012 Massimiliano Vurro - Antnio Landes 13. um dos monmeros na produos de biberes empolicarbonato A substncia pode migrar para o leite (ou outroslquidos) atravs dos biberesquando o plstico se desgasta(provocado frequentemente pela repetio dos ciclos dela