Mechanism of foetal wastage following immunoneutralization of riboflavin carrier protein in the pregnant rat: disturbances in flavin coenzyme levels.
Immunoneutralization of maternal RCP results in a greater than 90% decrease in the content and the incorporation of [2-14C]riboflavin into embryonic FAD as well as a percentage redistribution of both embryonic FMN and riboflavin. This is unaccompanied by any discernible changes in flavin distribution pattern in the maternal liver. Embryonic alpha-glycerophosphate dehydrogenase and NADPH-cytochrome c reductase register significant decreases in activities in the RCP antiserum-treated rats. These alterations readily explain the arrest of foetal growth culminating in pregnancy termination in the antiserum-treated animals.
D000818:Animals; D002352:Carrier Proteins / Q000502:physiology*; D005260:Female; D005313:Fetal Death / Q000378:metabolism / Q000503:physiopathology*; D005333:Fetus / Q000378:metabolism; D005486:Flavin Mononucleotide / Q000378:metabolism; D005182:Flavin-Adenine Dinucleotide / Q000378:metabolism*; D008431:Maternal-Fetal Exchange; D026901:Membrane Transport Proteins; D011247:Pregnancy; D051381:Rats; D012256:Riboflavin / Q000378:metabolism
D002352:Carrier Proteins; D026901:Membrane Transport Proteins; C019079:riboflavin-binding protein; D005182:Flavin-Adenine Dinucleotide; D005486:Flavin Mononucleotide; D012256:Riboflavin