Abstract 1895 Poster Session IV, Tuesday, 5/4 (poster 310)

The pulmonary antioxident enzymes (AOE), specifically catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GP), demonstrate a late gestational developmental pattern similar to that of surfactant and play an important role in lung biology during the perinatal period. Prenatal TRH treatment accelerates fetal lung surfactant maturation but inhibits maturation of AOE activity. It remains unclear whether TRH-induced inhibition of fetal lung AOE maturation involves thyroidal or extra-thyroidal mechanisms, an issue which can be explored using a mouse model for primary hypothyroidism. Primary hypothyroidism in the hyt/hyt mouse is due to a point mutation (Pro-556-Leu) in the B subunit of the TSH receptor of the Balb-c mouse and is transmitted as an autosomal recessive trait. The present study was designed to examine the effect of maternal treatment with TRH on AOE activity in hypothyroid fetal (E18) and newborn (NBR, P1) offspring, using the hyt/hyt mouse. Hyt/hyt mice made euthyroid by T3 supplementation were mated to carry hyt/hyt pups. Normal saline (NS) or TRH (0.6 mg/kg/dose) was administered to either hyt/hyt or balb-c mothers (I.P.) on E 16 and 17 (b.i.d.) & on E 18 of pregnancy 1 h before killing. Fetal or NBR lung AOE activities were quantitated by standard spectrophotometric assays. All data mean ±SEM, *p< 0.05 vs. appropriate control (ANOVA). (Table)

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Similar changes were found when AOE were expressed per mg DNA rather than protein. Results indicate that: 1) TRH inhibits fetal lung AOE activity maturation to the same extent in euthyroid (Balb-c) and hypothyroid (hyt/hyt) mice, suggesting that TRH induced inhibition of fetal lung AOE takes place via extra-thyroidal mechanisms; and 2) primary hypothyroidism inhibits neonatal but not fetal lunh AOE activity.