Retinoic acid: its biosynthesis and metabolism.

摘要: This article presents a model that integrates the functions of retinoid-binding proteins with retinoid metabolism. One these proteins, widely expressed (throughout target tissues and in all vertebrates) highly conserved cellular retinol-binding protein (CRBP), sequesters rctinol an internal binding pocket segregates it from intracellular milieu. The CRBP-retinol complex appears to be quantitatively major form retinol vivo , may protect promiscuous substrate nonenzymatic degradation and/or nonspecific enzymes. For example, at least seven types dehydrogenases catalyze retinal synthesis unbound vitro (NAD + vs. NADP dependent, cy-tosolic microsomal, short-chain dehydrogenases/reductases medium-chain alcohol dehydrogenases). But only fraction (some dehydrogenases/reductases) have fascinating additional ability catalyzing CRBP-bound as well. Similarly, CRBP other function esters, reduction generated intestinal β-carotene metabolism, retinoic acid discussion details evidence supporting integrated protein/metabolism. Also addressed are retinoid—androgen interactions incompatible ethanol causing fetal syndrome by competing directly dehydrogenation impair biosynthesis.