{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T19:14:36Z","timestamp":1792955676980,"version":"4.5.0"},"reference-count":42,"publisher":"SAGE Publications","issue":"12","license":[{"start":{"date-parts":[[2008,12,1]],"date-time":"2008-12-01T00:00:00Z","timestamp":1228089600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:p>\n                    Nuclear factor erythroid 2\u2013related factor 2 (Nrf2) is a transcription factor that is important in protection against oxidative stress. This study was designed to determine the role of Nrf2 signaling in transcriptional activation of detoxifying and antioxidant genes in an\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    mouse fetal alcohol syndrome model. Maternal ethanol treatment was found to increase both Nrf2 protein levels and Nrf2-ARE binding in mouse embryos. It also resulted in a moderate increase in the mRNA expression of Nrf2 downstream target detoxifying and antioxidant genes as well as an increase in the expression of antioxidant proteins. Pretreatment with the Nrf2 inducer, 3H-1,2 dithiole-3-thione (D3T), significantly increased Nrf2 protein levels and Nrf2-ARE binding, and strongly induced the mRNA expression of Nrf2 downstream target genes. It also increased the expression of antioxidant proteins and the activities of the antioxidant enzymes. Additionally, D3T pretreatment resulted in a significant decrease in ethanol-induced reactive oxygen species generation and apoptosis in mouse embryos. These results demonstrate that Nrf2 signaling is involved in the induction of antioxidant response in ethanol-exposed embryos. In addition, the potency of D3T in inducing antioxidants as well as in diminishing ethanol-induced apoptosis suggests that further exploration of the antiteratogenic effect of this compound will be fruitful.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    11, 2023\u20132033.\n                  <\/jats:p>","DOI":"10.1089\/ars.2007.2019","type":"journal-article","created":{"date-parts":[[2008,9,26]],"date-time":"2008-09-26T07:08:30Z","timestamp":1222412910000},"page":"2023-2033","source":"Crossref","is-referenced-by-count":213,"title":["Nrf2-Mediated Transcriptional Induction of Antioxidant Response in Mouse Embryos Exposed to Ethanol\n                    <i>in vivo<\/i>\n                    : Implications for the Prevention of Fetal Alcohol Spectrum Disorders"],"prefix":"10.1177","volume":"10","author":[{"given":"Jian","family":"Dong","sequence":"first","affiliation":[{"name":"University of North Carolina at Chapel Hill"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathleen K.","family":"Sulik","sequence":"additional","affiliation":[{"name":"University of North Carolina at Chapel Hill"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shao-yu","family":"Chen","sequence":"additional","affiliation":[{"name":"University of North Carolina at Chapel Hill"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2008,12,1]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0892-0362(95)98055-6"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1080\/109374001301419737"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/cne.21095"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuro.2006.07.019"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1177\/153537020623100809"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.081082098"},{"key":"e_1_3_3_8_2","first-page":"535","article-title":"Ethanol induces Fas\/Apo [apoptosis]-1 mRNA and cell suicide in the developing cerebral cortex","volume":"24","author":"Cheema ZF","year":"2000","unstructured":"Cheema ZF, , West JR, , Miranda RC. 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Generation of radical oxygen species by neural crest cells treated in vitro with isotretinoin and 4-oxoisotretinoin. 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