Abstract
The biochemical defect responsible for neonatal non-hæmolytic unconjugated hyperbilirubinæmia ("physiological" jaundice) in man is believed to be immaturity of uridine diphosphoglucuronyl transferase. An alternate hypothesis is that neonatal jaundice results from defective hepatic uptake of bilirubin due to deficiency of an intracellular organic anion-binding protein. The development of two hepatic cytoplasmic organic anion acceptor proteins, Y and Z, was investigated in guineapigs of various ages. Relative deficiency of Y, the major binding protein, was seen in fetal and newborn animals.
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