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001-es BibID:	BIBFORM036665
Első szerző:	Elmazar, Mohamed M. A.
Cím:	RARalpha-Mediated Teratogenicity in Mice Is Potentiated by an RXR Agonist and Reduced by an RAR Antagonist : dissection of Retinoid Receptor-Induced Pathways / Elmazar M. M., Rühl R., Reichert U., Shroot B., Nau H.
Dátum:	1997
ISSN:	0041-008X
Megjegyzések:	To dissect the complex pattern of retinoid-induced developmental defects, an RXR-selective agonist (AGN191701, an arylpropenyl-thiophene-carboxylic acid derivative) was coadministered with an RARalpha-selective agonist (Am580, an arylcarboxamidobenzoic acid derivative) to NMRI mice on Day 8.25 of gestation. AGN191701 was neither fetotoxic nor teratogenic at the doses used, but potentiated Am580-induced resorptions, spina bifida aperta, micrognathia, kidney hypoplasia, dilated bladder, undescended testis, atresia ani, tail malformations, fused ribs, and fetal weight retardation. These effects were generally reduced by coadministration of an RAR-selective antagonist (CD2366, an adamantyl-methoxyphenyl-heptatrienoic acid derivative). The incidence of other defects induced by an RARalpha-selective agonist such as exencephaly or cleft palate was neither greatly affected by the RXR-selective agonist nor by the antagonist. These results suggest that some malformations such as the posterior neural tube defect spina bifida as well as urogenital defects may be mediated via liganded RARalpha-RXR heterodimerization, while other defects such as the anterior neural tube defect exencephaly as well as cleft palate are induced by different mechanisms.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Toxicology And Applied Pharmacology. - 146 : 1 (1997), p. 21-28. -
További szerzők:	Rühl, Ralph (1969-) (vegyész) Reichert, Uwe Shroot, B. Nau, Heinz
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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