Congenital hereditary non-conjugate hyperbilirubinemias include Gilbert’s syndrome, Crigler-Najjar type 1 and 2 syndromes (or Arias’ disease). They are caused by a deficiency of the enzyme - bilirubinuridine-5’-diphosphate glucuronosyltransferase (UGT1A1), involved in glucuronization bilirubin. The is due to mutations UGT1A1 gene, which provides activity. Complete or almost complete loss (Crigl...

Non-diffusible residues in the medium were obtained from stationary-phasespent culture medium from Pseudomoms no. 95 by thorough dialysis and freeze-drying. These were added to other cultures at the start of growth and the distribution of 14C between EDTAextractable lipopolysaccharides, non-EDTA-extractable lipopolysaccharides, the remainder of the bacterium and the culture fluid was determined.

Gilbert and Crigler-Najjar syndromes are familial unconjugated hyperbilirubinemias caused by genetic lesions involving a single complex locus encoding for bilirubin UDP-glucuronosyltransferase (UGT1A1) gene. Over the last years a number of different mutations affecting this gene have been characterized. In this report is provided a summary of reported Gilbert and Crigler-Najjar syndromes associ...

Male and female Wistar rats with high and low hepatic microsomal UDP-glucuronosyltransferase activity towards androsterone were classified by partial hepatectomy. The breeding experiments between the classified high-activity and low-activity rats show that the genetic expression of the high transferase activity is inherited in an autosomal dominant fashion.