Chemoprevention of Neonatal Jaundice: Potency of Tin-Protoporphyrin in an Animal Model

• Published in: Science (American Association for the Advancement of Science) Vol. 217; no. 4566; pp. 1250 - 1252
• Main Authors: Drummond, George S., Kappas, Attallah
• Format: Journal Article
• Language: English
• Published: United States The American Association for the Advancement of Science 24.09.1982; American Association for the Advancement of Science
• Subjects: Animals; Atoms; Bile pigments; Bilirubin - blood; Cell lines; Disease Models, Animal; Diseases; Dosage; Heme Oxygenase (Decyclizing) - antagonists & inhibitors; Humans; Infant, Newborn; Infants (Newborn); Ions; Jaundice, Neonatal - prevention & control; Kidney - enzymology; Liver - enzymology; Metalloporphyrins; Mixed Function Oxygenases - antagonists & inhibitors; Molecules; Neonatal diseases; Neonatal jaundice; Newborns; Porphyrins; Porphyrins - therapeutic use; Protoporphyrins - pharmacology; Protoporphyrins - therapeutic use; Rats; Spleen; Spleen - enzymology; Tin - pharmacology; Tin - therapeutic use
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.6896768

The substantial increases of hepatic, splenic, and renal heme oxygenase levels that occur shortly after birth in neonatal rats were prevented by a single administration of tin-protoporphyrin (10 micromoles per kilogram of body weight). With this treatment serum bilirubin levels declined within 24 hours to near-normal adult levels and remained low throughout the postnatal period. Zinc-protoporphyrin at doses up to 50-fold greater than the effective dose of tin-protoporphyrin did not prevent the immediate increases in tissue heme oxygenase activities and in serum bilirubin levels that occur postnatally. Studies in vitro with microsomal heme oxygenase in human spleen indicate that tin-protoporphyrin is a potent competitive inhibitor of the oxidation of heme to bile pigment in this tissue.