{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T08:06:46Z","timestamp":1784794006081,"version":"3.55.0"},"reference-count":54,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,2,22]],"date-time":"2006-02-22T00:00:00Z","timestamp":1140566400000},"content-version":"vor","delay-in-days":21,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Birth Defects Research Pt B"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>BACKGROUND:<\/jats:bold> Animal models are necessary to investigate the mechanism of alcohol\u2010induced birth defects. We have used Japanese medaka (<jats:italic>Oryzias latipes<\/jats:italic>) as a non\u2010mammalian model to elucidate the molecular mechanism(s) of ethanol teratogenesis. <jats:bold>METHODS:<\/jats:bold> Medaka eggs, within 1\u2009hr post\u2010fertilization (hpf) were exposed to waterborne ethanol (0\u20131000\u2009mM) in hatching solution for 48\u2009hr. Embryo development was observed daily until 10 days post\u2010fertilization (dpf). The concentration of embryonic ethanol was determined enzymatically. Cartilage and bones were stained by Alcian blue and calcein, respectively and skeletal and cardiovascular defects were assessed microscopically. Genetic gender of the embryos was determined by PCR. Levels of two isoenzymes of alcohol dehydrogenase (Adh) mRNAs were determined by semi\u2010quantitative and real\u2010time RT\u2010PCR. <jats:bold>RESULTS:<\/jats:bold> The concentration of ethanol required to cause 50% mortality (LC<jats:sub>50<\/jats:sub>) in 10\u2009dpf embryos was 568\u2009mM, however, the embryo absorbed only 15\u201320% of the waterborne ethanol at all ethanol concentrations. The length of the lower jaw and calcification in tail fin cartilaginous structures were reduced by ethanol exposure. Active blood circulation was exhibited at 50+ hpf in embryos treated with 0\u2013100\u2009mM ethanol; active circulation was delayed and blood clots developed in embryos treated with 200\u2013400\u2009mM ethanol. The deleterious effects of ethanol were not gender\u2010specific. Moreover, ethanol treatment was unable to alter the constitutive expression of either Adh5 or Adh8\u2009mRNA in the medaka embryo. <jats:bold>CONCLUSIONS:<\/jats:bold> Preliminary results suggested that embryogenesis in medaka was significantly affected by ethanol exposure. Phenotypic features normally associated with ethanol exposure were similar to that observed in mammalian models of fetal alcohol syndrome. The results further indicated that medaka embryogenesis might be used as an alternative non\u2010mammalian model for investigating specific alterations in gene expression as a means to understand the molecular mechanism(s) of ethanol\u2010induced birth defects. <jats:italic>Birth Defects Res (Part B)<\/jats:italic> 77:29\u201339, 2006. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/bdrb.20072","type":"journal-article","created":{"date-parts":[[2006,2,22]],"date-time":"2006-02-22T19:16:53Z","timestamp":1140635813000},"page":"29-39","source":"Crossref","is-referenced-by-count":31,"title":["Japanese medaka (<i>Oryzias latipes<\/i>): developmental model for the study of alcohol teratology"],"prefix":"10.1002","volume":"77","author":[{"given":"Xueqing","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin","family":"Williams","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary L.","family":"Haasch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Asok 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