IN man and in other mammals, bilirubin is excreted in conjugated form, mainly as the glucuronide. Since in mammalian fœtal liver the enzymatic mechanism for glucuronide formation is poorly developed, reaching its full capacity only after birth, transient hyperbilirubinæmia is frequently observed during the neonatal period1. In the amphibian genus, Rana, hepatic glucuronide formation is absent in the larva, but present in the adult2. The larval forms undergo extra-uterine development and hence are readily accessible. These Amphibia would represent an excellent experimental model for studying various aspects of neonatal hyperbilirubinæmia, if it could be established that they, like mammals, excrete bilirubin as glucuronide. Therefore, we have examined amphibian bile pigment excretion to determine, first, whether in the adult Rana bilirubin is excreted as a glucuronide; secondly, whether metamorphosis is associated with qualitative or quantitative changes in pigment excretion; and thirdly, whether the excreted pigment is biliverdin, as has been postulated previously3, bilirubin, or another pigment.
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European Journal of Pediatrics (1981)