Abstract
GLUCURONIDE conjugates are formed by the condensation of an alcohol or acid aglycone with uridine diphosphoglucuronic acid by the enzyme, glucuronosyl transferase1. A functional immaturity of this enzyme system and perhaps a deficiency of uridine diphosphoglucuronic acid has been observed in new-born animals2. Since indirect-reacting bilirubin is converted to bilirubin glucuronide by means of glucuronosyl transferase3, Billing et al. 4 have suggested that physiological hyperbilirubinæmia of the new-born infant might be the result of a deficiency of this enzyme system. Recently, Lathe and Walker5 reported inhibition of bilirubin conjugation in liver slices by serum of pregnant women. This communication reports studies aimed at identifying the inhibitor substances and assessing their importance in hyperbilirubinæmia of the new-born.
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References
Dutton, G. J., and Storey, I. D. E., Biochem. J., 57, 275 (1954). Storey, I. D. E., and Dutton, G. J., ibid., 59, 279 (1955). Dutton, G. J., ibid., 64, 693 (1956).
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Savard, K., “Recent Prog. Hormone Res.”, 9, 185 (1954).
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YI-YUNG HSIA, D., DOWBEN, R., SHAW, R. et al. Inhibition of Glucuronosyl Transferase by Progestational Agents from Serum of Pregnant Women. Nature 187, 693–694 (1960). https://doi.org/10.1038/187693a0
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DOI: https://doi.org/10.1038/187693a0
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