Sudden death of chicken embryos with hereditary riboflavin deficiency.
Riboflavin-binding protein (RfBP) mediates the deposition of riboflavin during the formation of eggs in birds. Hens of a strain of Single-Comb White Leghorn chickens, which are genetically unable to produce RfBP, lay eggs containing insufficient riboflavin to sustain embryogenesis beyond 13 or 14 d of incubation. Embryos in these eggs grow normally until the day of death, and their heart rate is normal to within an hour of death. The effects of riboflavin-deficiency first appear after d 10 of incubation when embryos become severely hypoglycemic and begin to accumulate intermediates of fatty acid oxidation. Although the activities of flavin-dependent enzymes are reduced generally, the 80% reduction in the activity of medium-chain acyl-CoA dehydrogenase further suggests that the major metabolic consequence of riboflavin deficiency is a severe impairment of fatty acid oxidation. The riboflavin-deficient strain provides numerous insights into the metabolism of normal hens and chicken embryos and may be a useful model for sudden death syndromes in humans.
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Department of Chemistry and Biochemistry, University of Delaware, Newark, DE 19716, USA.
D044944:Acyl-CoA Dehydrogenases / Q000378:metabolism; D000818:Animals; D002642:Chick Embryo / Q000502:physiology*; D010084:Oxidation-Reduction; D012257:Riboflavin Deficiency / Q000150:complications*
D044944:Acyl-CoA Dehydrogenases