Vitamin A prevents inner ear defects in mice with congenital homeobox gene deficiency.

摘要: For the past 75 years, vitamin A and its biologically active metabolites, retinoids, have been object of intense study in biology medicine. large body evidence demonstrates that these nutrients are essential for normal development survival vertebrate embryos, including mammals. In fact, it has known since mid-1930s deficiency during pregnancy results death fetus congenital abnormalities. Similarly, excess dietary intake can also cause teratogenic responses. Among main targets both retinoid-induced teratogenesis heart, limbs, craniofacial structures, central nervous system, inner ear. Specific malformations induced a stage- dose-dependent manner. Thus, studies indicate precise levels timing action metabolites required patterning embryonic structures. addition, discovery nuclear receptors retinoic acid (RA) other derivatives provided molecular basis to explain how distinct doses compounds elicit cell-specific responses via direct transcriptional activation panel target genes.