Effect of premature birth and survival on hepatic thyroxine 5'-monodeiodinase activity in baboons.

Plasma thyroid hormones and hepatic 5'-monodeiodinase type I (5'-MDI) activity were measured in a primate model of premature birth and survival. When prematurely delivered at 140 days (term gestation is 184 days), infant baboons developed hyaline membrane disease, had no surge in T3 and T4, temporarily developed hypothyroxinemia, and had extremely low T3 concentrations during the first 40 h of life. After 4 days, both plasma T4 and T3 levels progressively increased, but were still considerably lower at 16 days compared to those in normal term infants. Hepatic 5'-MDI activity was measured in the presence of dithiothreitol in fetal, premature, and infant baboons. Fetal baboons at 140 and 161 days gestation had 80% less 5'-MDI activity than term infants, but at 178-180 days gestation, near term, fetal hepatic 5'-MDI activity increased to levels similar to those in young adults. Interruption of in utero development by premature birth resulted in no change in hepatic 5'-MDI activity after 24 h, but within 6 days after delivery, hepatic 5'-MDI had significantly increased to levels observed in fetal baboons near term. Kinetic analysis revealed that fetal and premature 5'-MDI had different maximum velocities and similar apparent Km values. There was no significant difference in hepatic total, protein, or nonprotein sulfhydryl groups between 1- and 10-day-old premature (140 days gestation) baboons. These results suggest that premature birth does not limit the postnatal maturation of hepatic 5'-MDI activity.