Effect of maternal/fetal vitamin A deficiency on fetal rat lung surfactant protein expression and the response to prenatal dexamethasone

Abstract

The purpose of this work was to determine whether maternal/fetal vitamin A deficiency in vivo had an effect on fetal lung surfactant protein expression and its response to antenatal maternal dexamethasone (DEX). Weanling female rats at 21 d (30-35 g) were fed control (C) (4 mg of vitamin A/kg of diet) or a vitamin A-deficient (D) (0.06 of mg vitamin A/kg) diet. These females were mated, and at selected pregnancy dates fetal and maternal tissues were obtained. Control mothers had liver retinyl palmitate (RP) concentrations of 246 ± 32 nmol/g of wet weight; those in the D group had 6.1 ± 2.9 nmol/g of wet weight. Control fetal liver RP was 12-fold higher and control fetal lung RP was 3-fold higher than in the D group (liver: 18.5 ± 0.4 nmol/g versus 1.5 ± 0.25 nmol/g; lung: 1.8 ± 0.98 nmol/g versus 0.6 ± 0.2 nmol/g). Neither fetal lung surfactant protein (SP)-C mRNA nor SP-A mRNA was affected by vitamin A deficiency. In a second experiment, pregnant rats from both C and D groups were injected with either DEX (1 mg/kg) or an equal volume of saline on d 15-17, and killed on d 18. DEX increased fetal lung SP-C mRNA 2-fold over the level found in the saline-injected group (saline, 1.0 ±0.2 versus DEX, 2.1 ± 0.2, p < 0.02). This increase in SP-C mRNA also occurred in fetal lungs from the D group (saline, 1.8 ± 0.4 versus DEX 3.7 ± 0.2, p < 0.01). Retinoic acid receptor-β mRNA, which responds to vitamin A levels and DEX in many systems, was lower in fetal lungs of the D group that had been treated with DEX. We conclude that fetal rat lung development, as measured by SP-C mRNA and SP-A mRNA, and the SP-C mRNA response to DEX, was not affected by vitamin A deficiency.