Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
1998-12-16
pubmed:abstractText
Vitamin A is required for reproduction and normal embryonic development. We have determined that all-trans-retinoic acid (atRA) can support development of the mammalian embryo to parturition in vitamin A-deficient (VAD) rats. At embryonic day (E) 0.5, VAD dams were fed purified diets containing either 12 micrograms of atRA per g of diet (230 micrograms per rat per day) or 250 micrograms of atRA per g of diet (4.5 mg per rat per day) or were fed the purified diet supplemented with a source of retinol (100 units of retinyl palmitate per day). An additional group was fed both 250 micrograms of atRA per g of diet in combination with retinyl palmitate. Embryonic survival to E12.5 was similar for all groups. However, embryonic development in the group fed 12 micrograms of atRA per g of diet was grossly abnormal. The most notable defects were in the region of the hindbrain, which included a loss of posterior cranial nerves (IX, X, XI, and XII) and postotic pharyngeal arches as well as the presence of ectopic otic vesicles and a swollen anterior cardinal vein. All embryonic abnormalities at E12.5 were prevented by feeding pharmacological amounts of atRA (250 micrograms/g diet) or by supplementation with retinyl palmitate. Embryos from VAD dams receiving 12 micrograms of atRA per g of diet were resorbed by E18.5, whereas those in the group fed 250 micrograms of atRA per g of diet survived to parturition but died shortly thereafter. Equivalent results were obtained by using commercial grade atRA or atRA that had been purified to eliminate any potential contamination by neutral retinoids, such as retinol. Thus, 250 micrograms of atRA per g of diet fed to VAD dams (approximately 4.5 mg per rat per day) can prevent the death of embryos at midgestation and prevents the early embryonic abnormalities that arise when VAD dams are fed insufficient amounts of atRA.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1159522, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-13030424, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1346922, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1353982, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1359423, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1361214, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-14116018, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-14139606, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-1528265, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-2739735, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-3293998, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-3624404, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-3702709, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-389569, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-4318536, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-5642194, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-6858941, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-7302873, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-7502242, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-7607067, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-7780180, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-7925028, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8041768, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8048045, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8096385, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8287543, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8287791, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8448410, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8521510, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8562696, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-8723346, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-9053316, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-9272952, http://linkedlifedata.com/resource/pubmed/commentcorrection/9811822-9463359
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
95
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13459-64
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Defects in embryonic hindbrain development and fetal resorption resulting from vitamin A deficiency in the rat are prevented by feeding pharmacological levels of all-trans-retinoic acid.
pubmed:affiliation
School of Pharmacy, University of Wisconsin, Madison, WI 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.