Publication | Closed Access
Chemoprevention of Neonatal Jaundice: Potency of Tin-Protoporphyrin in an Animal Model
107
Citations
21
References
1982
Year
Redox BiologyOxidative StressSingle AdministrationSerum Bilirubin LevelsToxicologyClinical ChemistryNeonatal RatsHealth SciencesAllergyBiochemistryLiver PhysiologyAnimal ModelNeonatal JaundiceHeme HomeostasisPharmacologyPorphyriasHepatologyHeme DegradationPhysiologyMetabolismMedicine
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.
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