Epigenetic responses following maternal dietary exposure to physiologically relevant levels of bisphenol A
dc.contributor.author | Anderson, Olivia S. | en_US |
dc.contributor.author | Nahar, Muna S. | en_US |
dc.contributor.author | Faulk, Christopher | en_US |
dc.contributor.author | Jones, Tamara R. | en_US |
dc.contributor.author | Liao, Chunyang | en_US |
dc.contributor.author | Kannan, Kurunthachalam | en_US |
dc.contributor.author | Weinhouse, Caren | en_US |
dc.contributor.author | Rozek, Laura S. | en_US |
dc.contributor.author | Dolinoy, Dana C. | en_US |
dc.date.accessioned | 2012-06-15T14:33:33Z | |
dc.date.available | 2013-08-01T14:04:39Z | en_US |
dc.date.issued | 2012-06 | en_US |
dc.identifier.citation | Anderson, Olivia S.; Nahar, Muna S.; Faulk, Christopher; Jones, Tamara R.; Liao, Chunyang; Kannan, Kurunthachalam; Weinhouse, Caren; Rozek, Laura S.; Dolinoy, Dana C. (2012). "Epigenetic responses following maternal dietary exposure to physiologically relevant levels of bisphenol A." Environmental and Molecular Mutagenesis 53(5): 334-342. <http://hdl.handle.net/2027.42/91363> | en_US |
dc.identifier.issn | 0893-6692 | en_US |
dc.identifier.issn | 1098-2280 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/91363 | |
dc.description.abstract | Animal studies have linked perinatal bisphenol A (BPA) exposure to altered DNA methylation, but little attention is given to analyzing multiple physiologically relevant doses. Utilizing the viable yellow agouti ( A vy ) mouse, we examine the effects of developmental exposure through maternal diet to 50 ng BPA/kg ( n = 14 litters), 50 μg BPA/kg ( n = 9 litters), or 50 mg BPA/kg ( n = 13 litters) on global and candidate gene methylation at postnatal day 22. Global methylation analysis reveals hypermethylation in tail tissue of a/a and A vy /a offspring across all dose groups compared with controls ( n = 11 litters; P < 0.02). Analysis of coat color phenotype replicates previous work showing that the distribution of 50 mg BPA/kg A vy /a offspring shifts toward yellow ( P = 0.006) by decreasing DNA methylation in the retrotransposon upstream of the Agouti gene ( P = 0.03). Maternal exposure to 50 μg or 50 ng BPA/kg, however, results in altered coat color distributions in comparison with control ( P = 0.04 and 0.02), but no DNA methylation effects at the Agouti gene are noted. DNA methylation at the CDK5 activator‐binding protein ( Cabp IAP ) metastable epiallele shows hypermethylation in the 50 μg BPA/kg offspring, compared with controls ( P = 0.02). Comparison of exposed mouse liver BPA levels to human fetal liver BPA levels indicates that the three experimental exposures are physiologically relevant. Thus, perinatal BPA exposure affects offspring phenotype and epigenetic regulation across multiple doses, indicating the need to evaluate dose effects in human clinical and population studies. Environ. Mol. Mutagen. 2012. © 2012 Wiley Periodicals, Inc. | en_US |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Epigenetics | en_US |
dc.subject.other | Developmental Origins of Disease | en_US |
dc.subject.other | Viable Yellow Agouti ( a Vy ) Mouse | en_US |
dc.subject.other | Bisphenol A | en_US |
dc.subject.other | DNA Methylation | en_US |
dc.title | Epigenetic responses following maternal dietary exposure to physiologically relevant levels of bisphenol A | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbsecondlevel | Genetics | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Otolaryngology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Wadsworth Center, New York State Department of Health and Department of Environmental Health Sciences, State University of New York at Albany, Albany, New York | en_US |
dc.contributor.affiliationother | 1415 Washington Heights, Ann Arbor, MI 48109‐2029, USA | en_US |
dc.identifier.pmid | 22467340 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/91363/1/21692_ftp.pdf | |
dc.identifier.doi | 10.1002/em.21692 | en_US |
dc.identifier.source | Environmental and Molecular Mutagenesis | en_US |
dc.identifier.citedreference | Rubin BS, Soto AM. 2009. Bisphenol A: Perinatal exposure and body weight. Mol Cell Endocrinol 304: 55 – 62. | en_US |
dc.identifier.citedreference | Dolinoy D, Weinhouse C, Jones T, Rozek L, Jirtle R. 2010. Variable histone modifications at the A (vy) metastable epiallele. Epigenetics 5: 637 – 644. | en_US |
dc.identifier.citedreference | Druker R, Bruxner TJ, Lehrbach NJ, Whitelaw E. 2004. Complex patterns of transcription at the insertion site of a retrotransposon in the mouse. Nucl Acids Res 32: 5800 – 5808. | en_US |
dc.identifier.citedreference | Duhl D, Vrieling H, Miller K, Wolff G, Barsh G. 1994. Neomorphic agouti mutations in obese yellow mice. Nat Genet 8: 59 – 65. | en_US |
dc.identifier.citedreference | Gallou‐Kabani C, Gabory A, Tost J, Karimi M, Mayeur S, Lesage J, Boudadi E, Gross M‐S, Taurelle J, Vigé A, Breton C, Reusens B, Remacle C, Vieau D, Ekström TJ, Jais J‐P, Junien C. 2010. Sex‐ and diet‐specific changes of imprinted gene expression and DNA methylation in mouse placenta under a high‐fat diet. PLoS ONE 5: e14398. | en_US |
dc.identifier.citedreference | Ginsberg G, Rice DC. 2009. Does rapid metabolism ensure negligible risk from bisphenol A? Environ Health Perspect 117: 1639 – 1643. | en_US |
dc.identifier.citedreference | Grunau C, Clark S, Rosenthal A. 2001. Bisulfite genomic sequencing: Systematic investigation of critical experimental parameters. Nucl Acids Res 29: E65 – 5. | en_US |
dc.identifier.citedreference | Heindel JJ, vom Saal FS. 2009. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Mol Cell Endocrinol 304: 90 – 96. | en_US |
dc.identifier.citedreference | Ho S‐M, Tang W‐Y, Belmonte de Frausto J, Prins GS. 2006. Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase Type 4 Variant 4. Cancer Res 66: 5624 – 5632. | en_US |
dc.identifier.citedreference | Honma S, Suzuki A, Buchanan DL, Katsu Y, Watanabe H, Iguchi T. 2002. Low dose effect of in utero exposure to bisphenol A and diethylstilbestrol on female mouse reproduction. Reprod Toxicol 16: 117 – 122. | en_US |
dc.identifier.citedreference | Jirtle RL, Skinner MK. 2007. Environmental epigenomics and disease susceptibility. Nat Rev Genet 8: 253 – 262. | en_US |
dc.identifier.citedreference | Kaminen‐Ahola N, Ahola A, Maga M, Mallitt K‐A, Fahey P, Cox T, Whitelaw E, Chong S. 2010. Maternal ethanol consumption alters the epigenotype and the phenotype of offspring in a mouse model. PLoS Genet. 6: e1000811. | en_US |
dc.identifier.citedreference | Karimi M, Johansson S, Ekstrm T. 2006. Using LUMA: A luminometric‐based assay for global DNA‐methylation. Epigenetics 1: 45 – 48. | en_US |
dc.identifier.citedreference | Kundakovic M, Champagne FA. 2011. Epigenetic perspective on the developmental effects of bisphenol A. Brain Behav Immunity 25: 1084 – 1093. | en_US |
dc.identifier.citedreference | Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D. 2008. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA 300: 1303 – 1310. | en_US |
dc.identifier.citedreference | Lee J‐J, Geli J, Larsson C, Wallin G, Karimi M, Zedenius J, Hg A, Foukakis T. 2008. Gene‐specific promoter hypermethylation without global hypomethylation in follicular thyroid cancer. Int J Oncol 33: 861 – 869. | en_US |
dc.identifier.citedreference | Miltenberger R, Mynatt R, Wilkinson J, Woychik R. 1997. The role of the agouti gene in the Yellow Obese Syndrome. J Nutr 127: 1902S – 1907S. | en_US |
dc.identifier.citedreference | Morgan H, Sutherland H, Martin D, Whitelaw E. 1999. Epigenetic inheritance at the agouti locus in the mouse. Nat Genet 23: 314 – 318. | en_US |
dc.identifier.citedreference | Moriyama K, Tagami T, Akamizu T, Usui T, Saijo M, Kanamoto N, Hataya Y, Shimatsu A, Kuzuya H, Nakao K. 2002. Thyroid hormone action is disrupted by bisphenol a as an antagonist. J Clin Endocrinol Metab 87: 5185 – 5190. | en_US |
dc.identifier.citedreference | Padmanabhan V, Siefert K, Ransom S, Johnson T, Pinkerton J, Anderson L, Tao L, Kannan K. 2008. Maternal bisphenol‐A levels at delivery: A looming problem? J Perinatol 28: 258 – 263. | en_US |
dc.identifier.citedreference | Poage GM, Houseman EA, Christensen BC, Butler RA, Avissar‐Whiting M, McClean MD, Waterboer T, Pawlita M, Marsit CJ, Kelsey KT. 2011. Global hypomethylation identifies loci targeted for hypermethylation in head and neck cancer. Clin Cancer Res 17: 3579 – 3589. | en_US |
dc.identifier.citedreference | Prins GS, Tang W‐Y, Belmonte J, Ho S‐M. 2008. Perinatal exposure to oestradiol and bisphenol A alters the prostate epigenome and increases susceptibility to carcinogenesis. Basic Clinical Pharmacol Toxicol 102: 134 – 138. | en_US |
dc.identifier.citedreference | Rakyan VK, Blewitt ME, Druker R, Preis JI, Whitelaw E. 2002. Metastable epialleles in mammals. Trends Genet 18: 348 – 351. | en_US |
dc.identifier.citedreference | Rubin BS, Murray MK, Damassa DA, King JC, Soto AM. 2001. Perinatal exposure to low doses of bisphenol A affects body weight, patterns of estrous cyclicity, and plasma LH levels. Environ Health Perspect 109: 675 – 680. | en_US |
dc.identifier.citedreference | Ruvinsky A, Flood W, Costantini F. 2001. Developmental mosaicism may explain spontaneous reappearance of the Axin(Fu) mutation in mice. Genesis 29: 49 – 54. | en_US |
dc.identifier.citedreference | Sieli PT, Jašarević E, Warzak DA, Mao J, Ellersieck MR, Liao C, Kannan K, Collet SH, Toutain P‐L, vom Saal FS, Rosenfeld CS. 2011. Comparison of serum bisphenol A concentrations in mice exposed to bisphenol a through the diet versus oral bolus exposure. Environ Health Perspect 119: 1260 – 1265. | en_US |
dc.identifier.citedreference | Takahashi O, Oishi S. 2003. Testicular toxicity of dietarily or parenterally administered bisphenol A in rats and mice. Food Chem Toxicol 41: 1035 – 1044. | en_US |
dc.identifier.citedreference | Vandenberg LN, Hauser R, Marcus M, Olea N, Welshons WV. 2007. Human exposure to bisphenol A (BPA). Reprod Toxicol 24: 139 – 177. | en_US |
dc.identifier.citedreference | Vandenberg LN, Maffini MV, Sonnenschein C, Rubin BS, Soto AM. 2009. Bisphenol‐A and the great divide: A review of controversies in the field of endocrine disruption. Endocrine Rev 30: 75 – 95. | en_US |
dc.identifier.citedreference | Vasicek T, Zeng L, Guan X, Zhang T, Costantini F, Tilghman S. 1997. Two dominant mutations in the mouse fused gene are the result of transposon insertions. Genetics 147: 777 – 786. | en_US |
dc.identifier.citedreference | Volkel W, Colnot T, Csanady G, Filser J, Dekant W. 2002. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chem Res Toxicol 15: 1281 – 1287. | en_US |
dc.identifier.citedreference | vom Saal FS, Welshons WV. 2006. Large effects from small exposures. II. The importance of positive controls in low‐dose research on bisphenol A. Environ Res 100: 50 – 76. | en_US |
dc.identifier.citedreference | Waterland R, Jirtle R. 2003. Transposable elements: Targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol 23: 5293 – 5300. | en_US |
dc.identifier.citedreference | Waterland R, Jirtle R. 2004. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Nutrition 20: 63 – 68. | en_US |
dc.identifier.citedreference | Barker DJ. 2004. The developmental origins of adult disease. J Am Coll Nut 23: 588 – 595. | en_US |
dc.identifier.citedreference | Bateson P, Barker D, Clutton‐Brock T, Deb D, D'Udine B, Foley RA, Gluckman P, Godfrey K, Kirkwood T, Lahr MM, McNamara J, Metcalfe NB, Monaghan P, Spencer HG, Sultan SE. 2004. Developmental plasticity and human health. Nature 430: 419 – 421. | en_US |
dc.identifier.citedreference | Bromer JG, Zhou Y, Taylor MB, Doherty L, Taylor HS. 2010. Bisphenol‐A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response. The FASEB J 24: 2273 – 2280. | en_US |
dc.identifier.citedreference | Calafat A, Ye X, Wong L, Reidy J, Needham L. 2008. Exposure of the U.S. population to bisphenol A and 4‐tertiary‐octylphenol: 2003–2004. Environ Health Perspect 116: 39 – 44. | en_US |
dc.identifier.citedreference | Cooney CA, Dave AA, Wolff GL. 2002. Maternal methyl supplements in mice affect epigenetic variation and DNA methylation of offspring. J Nutr 132: 2393 – 2400. | en_US |
dc.identifier.citedreference | Deneberg S, Grovdal M, Karimi M, Jansson M, Nahi H, Corbacioglu A, Gaidzik V, Dohner K, Paul C, Ekstrom TJ, Hellstrom‐Lindberg E, Lehmann S. 2010. Gene‐specific and global methylation patterns predict outcome in patients with acute myeloid leukemia. Leukemia 24: 932 – 941. | en_US |
dc.identifier.citedreference | Dolinoy DC, Wiedman J, Waterland R, Jirtle RL. 2006. Maternal genistein alters coat color and protects Avy mouse offspring from obesity by modifying the fetal epigenome. Environ Health Perspect 114: 567 – 572. | en_US |
dc.identifier.citedreference | Dolinoy DC, Huang D, Jirtle RL. 2007. Maternal nutrient supplementation counteracts bisphenol A‐induced DNA hypomethylation in early development. Proc Natl Acad Sci USA 104: 13056 – 13061. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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