Figure 7. Model of bilirubin mobilization by HSA administration.

In normal conditions, the bilirubin-binding capacity provided by albumin exceeds the amount of UCB (left). In severe hyperbilirubinemic conditions, UCB outnumbers the albumin-binding capacity, and the excess of UCB (free bilirubin) solubilizes in lipid-rich tissues, such as the brain and cerebellum (center), resulting in neurological damage. When plasma bilirubin-binding capacity is artificially increased by HSA administration, bilirubin is mobilized from tissues to the plasma compartment, resulting in safe levels of tissue UCB (right) and increased plasma UCB levels. Thus, bilirubin mobilization prevents neurological damage and rescues lethality in HSA-treated mutant mice UCB, unconjugated bilirubin; HSA, human serum albumin.