Zachman R D, Grummer M A
Department of Pediatrics, University of Wisconsin-Meriter Perinatal Center, Madison 53715, USA.
Pediatr Res. 1998 Feb;43(2):178-83. doi: 10.1203/00006450-199802000-00004.
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-beta 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.
这项研究的目的是确定母体/胎儿体内维生素A缺乏是否会影响胎儿肺表面活性物质蛋白的表达及其对产前母体地塞米松（DEX）的反应。21日龄（30 - 35克）的断奶雌性大鼠被喂食对照（C）（4毫克维生素A/千克饮食）或维生素A缺乏（D）（0.06毫克维生素A/千克）饮食。这些雌性大鼠交配后，在选定的妊娠日期获取胎儿和母体组织。对照母亲肝脏视黄醇棕榈酸酯（RP）浓度为246±32纳摩尔/克湿重；D组母亲为6.1±2.9纳摩尔/克湿重。对照胎儿肝脏RP比D组高12倍，对照胎儿肺RP比D组高3倍（肝脏：18.5±0.4纳摩尔/克对1.5±0.25纳摩尔/克；肺：1.8±0.98纳摩尔/克对0.6±0.2纳摩尔/克）。维生素A缺乏对胎儿肺表面活性物质蛋白（SP）-C mRNA和SP-A mRNA均无影响。在第二个实验中，C组和D组的怀孕大鼠在第15 - 17天注射DEX（1毫克/千克）或等体积的生理盐水，并在第18天处死。DEX使胎儿肺SP-C mRNA水平比注射生理盐水组增加了2倍（生理盐水组为1.0±0.2，DEX组为2.1±0.2，p < 0.02）。D组胎儿肺中SP-C mRNA也出现这种增加（生理盐水组为1.8±0.4，DEX组为3.7±0.2，p < 0.01）。在许多系统中对维生素A水平和DEX有反应的视黄酸受体-β mRNA，在接受DEX治疗的D组胎儿肺中较低。我们得出结论，以SP-C mRNA和SP-A mRNA衡量的胎鼠肺发育以及SP-C mRNA对DEX的反应不受维生素A缺乏的影响。
