EFFECT OF MATERNAL FETAL VITAMIN-A-DEFICIENCY ON FETAL-RAT LUNG SURFACTANT PROTEIN EXPRESSION AND THE RESPONSE TO PRENATAL DEXAMETHASONE/

The purpose of this work was to determine whether maternal/fetal vitam in 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 vitami n A/kg) diet. These females were mated, and at selected pregnancy date s fetal and maternal tissues were obtained. Control mothers had liver retinyl palmitate (RP) concentrations of 246 +/- 32 nmol/g of wet weig ht; 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-fol d 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). N either fetal lung surfactant protein (SP)-C mRNA nor SP-A mRNA was aff ected by vitamin A deficiency. In a second experiment, pregnant rats f rom 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 f etal 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 i ncrease in SP-C mRNA also occurred in fetal lungs from the D group (sa line, 1.8 +/- 0.4 versus DEX 3.7 +/- 0.2, p < 0.01). Retinoic acid rec eptor-beta mRNA, which responds to vitamin A levels and DEX in many sy stems, was lower in fetal lungs of the D group that had been treated w ith DEX. We conclude that fetal rat lung development, as measured by S P-C mRNA and SP-A mRNA, and the SP-C mRNA response to DEX, was not aff ected by vitamin A deficiency.