Hyperbilirubinemia is likely the most frequently diagnosed and treated condition in the newborn. Treatment is aimed at preventing the entry of bilirubin into the brain because of the risk of permanent neurologic damage (kernicterus). The mode by which bilirubin enters the brain, its metabolic fate after entry, and the biochemical basis of its toxicity are unknown. The congenitally jaundiced rat (Gunn strain) lacks glucuronyl transferase and develops unconjugated hyperbilirubinemia in the neonatal period. It provides a model for human neonatal jaundice. However, the genetic background of Gunn mutants varies from laboratory to laboratory. The Gunn strain has thus been transferred into two genetically defined backgrounds, RHA and ACI. We studied the two strains from birth through adolescence, following growth, survival, serum albumin, serum bilirubin, hematocrit, and liver glucuronyl transferase activities. Both strains are jaundiced in the neonatal period, with serum bilirubin levels peaking about two weeks of age. Survival of jaundiced (homozygotes) and nonjaundiced (heterozygotes) pups were essentially the same in both strains. However, survival of the ACI rats was low while that of the RHA was high. Thus, the RHA strain of congenitally jaundiced rats provides a useful model for the study of neonatal jaundice.
