{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:19:46Z","timestamp":1791285586448,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,6,18]],"date-time":"2012-06-18T00:00:00Z","timestamp":1339977600000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Nutrition Food Res"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:sec><jats:title>Scope<\/jats:title><jats:p>Prenatal folate and methyl donor malnutrition lead to epigenetic alterations that could enhance susceptibility to disease. Methyl\u2010deficient diet (<jats:styled-content style=\"fixed-case\">MDD<\/jats:styled-content>) and fumonisin <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 are risk factors for neural tube defects and cancers. Evidence indicates that <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 impairs folate metabolism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>Folate receptors and four heterochromatin markers were investigated in rat fetuses liver derived from dams exposed to <jats:styled-content style=\"fixed-case\">MDD<\/jats:styled-content> and\/or <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 administered at a dose twice higher than the provisional maximum tolerable daily intake (PMTDI = 2 \u03bcg\/kg\/day). Even though folate receptors transcription seemed up\u2010regulated by methyl depletion regardless of <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 treatment, combined <jats:styled-content style=\"fixed-case\">MDD\/FB<\/jats:styled-content>1 exposure might reverse this up\u2010regulation since folate receptors transcripts were lower in the <jats:styled-content style=\"fixed-case\">MDD\/FB<\/jats:styled-content>1 versus <jats:styled-content style=\"fixed-case\">MDD<\/jats:styled-content> group. Methyl depletion decreased <jats:styled-content style=\"fixed-case\">H4K<\/jats:styled-content>20me3. Combined <jats:styled-content style=\"fixed-case\">MDD\/FB<\/jats:styled-content>1 decreased <jats:styled-content style=\"fixed-case\">H4K<\/jats:styled-content>20me3 even more and increased <jats:styled-content style=\"fixed-case\">H3K<\/jats:styled-content>9me3. The elevated <jats:styled-content style=\"fixed-case\">H3K<\/jats:styled-content>9me3 can be viewed as a defense mechanism inciting the cell to resist heterochromatin disorganization. <jats:styled-content style=\"fixed-case\">H3R<\/jats:styled-content>2me2 and <jats:styled-content style=\"fixed-case\">H4K<\/jats:styled-content>16<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>c varied according to this mechanism even though statistical significance was not consistent.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Considering that humans are exposed to <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 levels above the <jats:styled-content style=\"fixed-case\">PMTDI<\/jats:styled-content>, this study is relevant because it suggests that low doses of <jats:styled-content style=\"fixed-case\">FB<\/jats:styled-content>1 interact with <jats:styled-content style=\"fixed-case\">MDD<\/jats:styled-content> thus contributing to disrupt the epigenetic landscape.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201100640","type":"journal-article","created":{"date-parts":[[2012,6,18]],"date-time":"2012-06-18T15:27:51Z","timestamp":1340033271000},"page":"976-985","source":"Crossref","is-referenced-by-count":40,"title":["Fumonisin <scp>FB<\/scp>1 treatment acts synergistically with methyl donor deficiency during rat pregnancy to produce alterations of <scp>H<\/scp>3\u2010 and <scp>H<\/scp>4\u2010histone methylation patterns in fetuses"],"prefix":"10.1002","volume":"56","author":[{"given":"H\u00e9l\u00e8ne","family":"Pellanda","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thierry","family":"Forges","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aude","family":"Bressenot","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abalo","family":"Chango","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Pierre","family":"Bronowicki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Louis","family":"Gu\u00e9ant","sequence":"additional","affiliation":[{"name":"INSERM U954 \u201cNutrition Genetics and Environmental Risk Exposure,\u201d Facult\u00e9 de M\u00e9decine Nancy Universit\u00e9 Vandoeuvre les Nancy France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fares","family":"Namour","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,6,18]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1128\/AEM.68.5.2101-2105.2002"},{"key":"e_1_2_7_3_1","doi-asserted-by":"crossref","first-page":"1806","DOI":"10.1128\/aem.54.7.1806-1811.1988","article-title":"Fumonisins\u2014novel mycotoxins with cancer\u2010promoting activity produced by \n                     Fusarium moniliforme","volume":"54","author":"Gelderblom W. 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